First name
Robert
Middle name
O
Last name
Wright

Title

Spatially and Temporally Resolved Ambient PM in Relation to Preterm Birth.

Year of Publication

2021

Date Published

2021 Dec 14

ISSN Number

2305-6304

Abstract

<p>Growing evidence suggests that maternal exposure to ambient fine particulate matter (PM) during pregnancy is associated with preterm birth; however, few studies have examined critical windows of exposure, which can help elucidate underlying biologic mechanisms and inform public health messaging for limiting exposure. Participants included 891 mother-newborn pairs enrolled in a U.S.-based pregnancy cohort study. Daily residential PM concentrations at a 1 × 1 km resolution were estimated using a satellite-based hybrid model. Gestational age at birth was abstracted from electronic medical records and preterm birth (PTB) was defined as &lt;37 completed weeks of gestation. We used Critical Window Variable Selection to examine weekly PM exposure in relation to the odds of PTB and examined sex-specific associations using stratified models. The mean ± standard deviation PM level averaged across pregnancy was 8.13 ± 1.10 µg/m. PM exposure was not associated with an increased odds of PTB during any gestational week. In sex-stratified models, we observed a marginal increase in the odds of PTB with exposure occurring during gestational week 16 among female infants only. This study does not provide strong evidence supporting an association between weekly exposure to PM and preterm birth.</p>

DOI

10.3390/toxics9120352

Alternate Title

Toxics

PMID

34941786

Title

Prenatal lead exposure and fetal growth: Smaller infants have heightened susceptibility.

Year of Publication

2017

Number of Pages

228-233

Date Published

2017 Feb

ISSN Number

1873-6750

Abstract

<p><strong>BACKGROUND: </strong>As population lead levels decrease, the toxic effects of lead may be distributed to more sensitive populations, such as infants with poor fetal growth.</p>

<p><strong>OBJECTIVES: </strong>To determine the association of prenatal lead exposure and fetal growth; and to evaluate whether infants with poor fetal growth are more susceptible to lead toxicity than those with normal fetal growth.</p>

<p><strong>METHODS: </strong>We examined the association of second trimester maternal blood lead levels (BLL) with birthweight-for-gestational age (BWGA) z-score in 944 mother-infant participants of the PROGRESS cohort. We determined the association between maternal BLL and BWGA z-score by using both linear and quantile regression. We estimated odds ratios for small-for-gestational age (SGA) infants between maternal BLL quartiles using logistic regression. Maternal age, body mass index, socioeconomic status, parity, household smoking exposure, hemoglobin levels, and infant sex were included as confounders.</p>

<p><strong>RESULTS: </strong>While linear regression showed a negative association between maternal BLL and BWGA z-score (β=-0.06 z-score units per log BLL increase; 95% CI: -0.13, 0.003; P=0.06), quantile regression revealed larger magnitudes of this association in the &lt;30th percentiles of BWGA z-score (β range [-0.08, -0.13] z-score units per log BLL increase; all P values&lt;0.05). Mothers in the highest BLL quartile had an odds ratio of 1.62 (95% CI: 0.99-2.65) for having a SGA infant compared to the lowest BLL quartile.</p>

<p><strong>CONCLUSIONS: </strong>While both linear and quantile regression showed a negative association between prenatal lead exposure and birthweight, quantile regression revealed that smaller infants may represent a more susceptible subpopulation.</p>

DOI

10.1016/j.envint.2016.11.023

Alternate Title

Environ Int

PMID

27923585

Title

Bacterial and cytokine mixtures predict the length of gestation and are associated with miRNA expression in the cervix.

Year of Publication

2017

Number of Pages

33-45

Date Published

2017 01

ISSN Number

1750-192X

Abstract

<p><strong>AIM: </strong>Bacterial vaginosis may lead to preterm birth through epigenetic programming of the inflammatory response, specifically via miRNA expression.</p>

<p><strong>METHODS: </strong>We quantified bacterial 16S rRNA, cytokine mRNA and 800 miRNA from cervical swabs obtained from 80 women at 16-19 weeks' gestation. We generated bacterial and cytokine indices using weighted quantile sum regression and examined associations with miRNA and gestational age at delivery.</p>

<p><strong>RESULTS &amp; DISCUSSION: </strong>Each decile of the bacterial and cytokine indices was associated with shorter gestations (p &lt; 0.005). The bacterial index was associated with miR-494, 371a, 4286, 185, 320e, 888 and 23a (p &lt; 0.05). miR-494 remained significant after false discovery rate correction (q &lt; 0.1). The cytokine index was associated with 27 miRNAs (p &lt; 0.05; q &lt; 0.01).</p>

<p><strong>CONCLUSION: </strong>Future investigation into the role of bacterial vaginosis- and inflammation-associated miRNA and preterm birth is warranted.</p>

DOI

10.2217/epi-2016-0095

Alternate Title

Epigenomics

PMID

27936911

Title

Prenatal Stress, Methylation in Inflammation-Related Genes, and Adiposity Measures in Early Childhood: the Programming Research in Obesity, Growth Environment and Social Stress Cohort Study.

Year of Publication

2018

Number of Pages

34-41

Date Published

2018 01

ISSN Number

1534-7796

Abstract

<p><strong>OBJECTIVE: </strong>Maternal stress during pregnancy may influence childhood growth and adiposity, possibly through immune/inflammatory programming. We investigated whether exposure to prenatal stress and methylation in inflammation-related genes were associated with childhood adiposity in 424 mother-child pairs in Mexico City, Mexico.</p>

<p><strong>METHODS: </strong>A stress index was created based on four prenatally administered stress-related scales (Exposure to Violence, Crisis in Family Systems, State-Trait Anxiety Inventory, and Edinburgh Postnatal Depression Scale). We measured weight, height, body fat mass (BFM), percentage body fat (PBF), and waist circumference in early childhood (age range, 4-6 years). Body mass index (BMI) z scores were calculated according to World Health Organization standards. DNA methylation in gene promoters of tumor necrosis factor α, interleukin 8, and interleukin 6 (IL6) in umbilical cord blood were determined by pyrosequencing.</p>

<p><strong>RESULTS: </strong>An interquartile range increase in stress index (27.3) was associated with decreases of 0.14 unit in BMI z score (95% confidence interval [CI] = -0.28 to -0.005), 5.6% in BFM (95% CI = -9.7 to -1.4), 3.5% in PBF (95% CI = -6.3 to -0.5), and 1.2% in waist circumference (95% CI = -2.4 to -0.04) in multivariable-adjusted models. An interquartile range increase in IL6 methylation (3.9%) was associated with increases of 0.23 unit in BMI z score (95% CI = 0.06-0.40), 8.1% (95% CI = 2.3-14.3) in BFM, 5.5% (95% CI = 1.7-9.5) in PBF, and 1.7% (95% CI = 0.2-3.3) in waist circumference.</p>

<p><strong>CONCLUSIONS: </strong>Prenatal stress was associated with decreased childhood adiposity, whereas cord blood IL6 methylation was associated with increased childhood adiposity in Mexican children.</p>

DOI

10.1097/PSY.0000000000000517

Alternate Title

Psychosom Med

PMID

28787364

Title

Maternal blood arsenic levels and associations with birth weight-for-gestational age.

Year of Publication

2019

Number of Pages

108603

Date Published

2019 Jul 22

ISSN Number

1096-0953

Abstract

<p><strong>BACKGROUND: </strong>Among highly exposed populations, arsenic exposure in utero may be associated with decreased birth weight, however less is known about potential effects of arsenic exposure in urban communities without contaminated sources such as drinking water.</p>

<p><strong>OBJECTIVE: </strong>Investigate the association of blood arsenic levels with birth weight-for-gestational age categories within a prospective birth cohort study.</p>

<p><strong>DESIGN/METHODS: </strong>We analyzed 730 mother-infant dyads within the Programming Research in Obesity, GRowth, Environment and Social Stressors (PROGRESS) cohort in Mexico City. Total arsenic was measured in maternal blood samples from the 2nd and 3rd trimesters, at delivery, as well as from infant umbilical cord blood samples. Multivariable, multinomial logistic regression. models adjusting for maternal age at enrollment, pre-pregnancy body mass index, parity, infant sex, socioeconomic position, and prenatal environmental tobacco smoke exposure were used to calculate odds ratios of small-for-gestational age (&lt;10th percentile, SGA) and large-for-gestational age (&gt;90th percentile, LGA) compared to appropriate-for-gestational age (AGA) per unit increase of log-transformed arsenic.</p>

<p><strong>RESULTS: </strong>Median (IQR) blood arsenic levels for maternal second trimester were 0.72 (0.33) μg/L, maternal third trimester 0.75 (0.41) μg/L, maternal at delivery 0.85 (0.70) μg/L, and infant cord 0.78 (0.65) μg/L. Maternal delivery and infant cord blood samples were most strongly correlated (spearman r = 0.65, p &lt; 0.0001). Maternal arsenic levels at delivery were associated with significantly higher odds of both SGA (adj. OR = 1.44, 95% CI: 1.08-1.93) and LGA (adj. OR = 2.03, 95% CI: 1.12-3.67) compared to AGA. Results were similar for cord blood. There were 130 SGA infants and 22 LGA infants. Earlier in pregnancy, there were no significant associations of arsenic and birth weight-for-gestational age. However, we observed non-significantly higher odds of LGA among women with higher arsenic levels in the 3rd trimester (adj. OR = 1.46, 95% CI: 0.67-3.12).</p>

<p><strong>CONCLUSION: </strong>We found that in a Mexico City birth cohort, higher maternal blood arsenic levels at delivery were associated with higher odds of both SGA and LGA. However, sources and species of arsenic were not known and the number of LGA infants was small, limiting the interpretation of this finding and highlighting the importance of future large studies to incorporate arsenic speciation. If our findings were confirmed in studies that addressed these limitations, determining modifiable factors that could be mitigated, such as sources of arsenic exposure, may be important for optimizing fetal growth to improve long-term health of children.</p>

DOI

10.1016/j.envres.2019.108603

Alternate Title

Environ. Res.

PMID

31357156

Title

Prenatal salivary sex hormone levels and birth-weight-for-gestational age.

Year of Publication

2019

Date Published

2019 May 20

ISSN Number

1476-5543

Abstract

<p><strong>OBJECTIVE: </strong>To determine whether prenatal sex hormones from maternal saliva are associated with birth-weight-for-gestational age.</p>

<p><strong>STUDY DESIGN: </strong>We measured salivary progesterone, testosterone, estradiol, dehydroepiandrosterone (DHEA), and cortisone in 504 pregnant women in a Mexico City cohort. We performed linear and modified Poisson regression to examine associations of log-transformed hormones with birth-weight-for-gestational age z-scores and the risk of small-for-gestational age (SGA) and large-for-gestational age (LGA) adjusting for maternal age, sex, BMI, parity, smoking, education, and socioeconomic status.</p>

<p><strong>RESULTS: </strong>In total, 15% of infants were SGA and 2% were LGA. Each interquartile range increment in testosterone/estradiol ratio was associated with a 0.12 decrement in birth-weight-for-gestational age z-score (95% CI: -0.27 to -0.02) and a 50% higher risk of SGA versus appropriate-for-gestational age (AGA) (95% CI: 1.13-1.99).</p>

<p><strong>CONCLUSION: </strong>Higher salivary testosterone/estradiol ratios may affect fetal growth, and identifying the predictors of hormone levels may be important to optimizing fetal growth.</p>

DOI

10.1038/s41372-019-0385-y

Alternate Title

J Perinatol

PMID

31110244

Title

Prenatal lead exposure modifies the effect of shorter gestation on increased blood pressure in children.

Year of Publication

2018

Number of Pages

464-471

Date Published

2018 Aug 23

ISSN Number

1873-6750

Abstract

<p><strong>BACKGROUND: </strong>High blood pressure (BP) in childhood is frequently renal in origin and a risk factor for adult hypertension and cardiovascular disease. Shorter gestations are a known risk factor for increased BP in adults and children, due in part to a nephron deficit in children born preterm. As nephrogenesis is incomplete until 36 weeks gestation, prenatal lead exposure occurring during a susceptible period of renal development may contribute to programming for later life renal disease. The relationship between shorter gestation and children's BP has not yet been explored to identify i) critical windows using nonlinear piecewise models or ii) combined with other early life risk factors such as prenatal lead exposure.</p>

<p><strong>OBJECTIVES: </strong>(1) To evaluate the nonlinear relationship between lower gestational age and childhood BP measured at 4-6 years of age, and (2) to investigate modification by prenatal lead exposure.</p>

<p><strong>METHODS: </strong>In a prospective longitudinal birth cohort, we assessed 565 children between 4 and 6 years of age (mean: 4.8 years) in the PROGRESS cohort in Mexico City, Mexico. Gestational age at delivery was calculated using maternal report of last menstrual period (LMP) and confirmed with Capurro physical examination at birth. We measured pregnant women's blood lead levels (BLLs) in the second trimester via inductively coupled plasma-mass spectrometry and children's BP using an automated device. We performed both linear and nonlinear piecewise regression analyses to examine associations of gestational age with children's BP adjusting for children's age, sex, height, prenatal exposure to smoke, and maternal socioeconomic status. We stratified to assess modification by prenatal lead exposure, and used a data-adaptive approach to identify a lead cutpoint.</p>

<p><strong>RESULTS: </strong>Maternal second trimester BLLs ranged from 0.7 to 17.8 μg/dL with 112 (20%) women above the CDC guideline level of 5 μg/dL. In adjusted linear regression models, a one week reduction in gestational age was associated with a 0.5 mm Hg (95%CI: 0.2, 0.8) increase in SBP and a 0.4 mm Hg (95%CI 0.1, 0.6) increase in DBP. Our nonlinear models suggested evidence for different magnitude estimates on either side of an estimated join-point at 35.9 weeks' gestation, but did not reach statistical significance. However, when stratified by prenatal lead exposure, we identified a cutpoint lead level of concern of 2.5 μg/dL that suggested an interaction between gestational age and blood lead. Specifically, for BLLs ≥ 2.5 μg/dL, SBP was 1.6 (95%CI: 0.3, 2.9) mm Hg higher per each week reduction in gestational age among children born before 37.0 weeks; and among children born after 37.0 weeks, this relationship was attenuated yet remained significant [β: 0.9, 95%CI (0.2, 1.6)]. At BLLs below 2.5 μg/dL, there was no appreciable association between lower gestational age and SBP.</p>

<p><strong>CONCLUSIONS: </strong>Our findings suggest that shorter gestation combined with higher prenatal lead exposure contributes to a higher risk of increased SBP at 4-6 years of age, particularly among infants born &lt;37 weeks gestation. Our results underscore the importance of preventing prenatal lead exposure - even levels as low as 2.5 μg/dL - especially among pregnant women at risk for preterm birth. Given that high BP in childhood is a risk factor for adult hypertension and cardiovascular disease later in life, these results may have implications that extend across the life span.</p>

DOI

10.1016/j.envint.2018.08.038

Alternate Title

Environ Int

PMID

30145310

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