Prenatal exposure to consumer product chemical mixtures and size for gestational age at delivery

Abstract Background While fetal growth is a tightly regulated process, it is sensitive to environmental exposures that occur during pregnancy. Many commonly used consumer products contain chemicals that can disturb processes underlying fetal growth. However, mixtures of these chemicals have been minimally examined. We investigated associations between prenatal exposure to 33 consumer product chemicals (nine organophosphate ester flame retardant [OPE] metabolites, 12 phthalate metabolites, and 12 phenols) and the odds of small- or large-for-gestational age (SGA and LGA) births. Methods This case-control study was comprised of SGA (N = 31), LGA (N = 28), and appropriate for gestational age control (N = 31) births selected from the larger LIFECODES cohort. Biomarkers of exposure to consumer product chemicals were quantified in maternal urine collected from up to three study visits during pregnancy. In a single-pollutant approach, odds ratios (OR) and 95% confidence intervals (CI) of SGA and LGA associated with an interquartile range (IQR)-increase in exposure biomarkers were estimated using multinomial logistic regression. In a multi-pollutant approach, quantile g-computation was used to jointly estimate the OR (95% CI) of SGA and LGA per simultaneous one quartile-change in all biomarkers belonging to each chemical class. Results Among the 33 biomarkers analyzed, 20 were detected in at least 50% of the participants. After adjusting for potential confounders, we observed reduced odds of LGA in association with higher urinary concentrations of several exposure biomarkers. For example, an IQR-increase in the OPE metabolite, diphenyl phosphate, was associated with lower odds of LGA (OR: 0.40 [95% CI: 0.18, 0.87]). Using quantile g-computation, we estimated lower odds of an LGA birth for higher OPE metabolite concentrations (OR: 0.49 [95% CI: 0.27, 0.89]) and phthalate metabolite concentrations (OR: 0.23 [95% CI: 0.07, 0.73]). Associations between consumer product chemicals and SGA were largely null. Conclusions Joint exposure to OPEs and phthalates was associated with lower odds of delivering LGA. Associations with LGA could indicate a specific impact of these exposures on the high end of the birth weight spectrum. Future work to understand this nuance in the associations between consumer product chemical mixtures and fetal growth is warranted.

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Prenatal exposure to consumer product chemical mixtures and size for gestational age at delivery

10.21203/rs.3.rs-47532/v2 ◽

2021 ◽

Author(s):

Paige A Bommarito ◽

Barrett M. Welch ◽

Alexander P Keil ◽

George P Baker ◽

Dave E Cantonwine ◽

...

Keyword(s):

Prenatal Exposure ◽

Fetal Growth ◽

Gestational Age ◽

Multinomial Logistic Regression ◽

Consumer Product ◽

Chemical Mixtures ◽

Lower Odds ◽

Exposure Biomarkers ◽

Metabolite Concentrations ◽

Phthalate Metabolite

Abstract Background: While fetal growth is a tightly regulated process, it is sensitive to environmental exposures that occur during pregnancy. Many commonly used consumer products contain chemicals that can disturb processes underlying fetal growth. However, mixtures of these chemicals have been minimally examined. We investigated associations between prenatal exposure to 33 consumer product chemicals (nine organophosphate ester flame retardant [OPE] metabolites, 12 phthalate metabolites, and 12 phenols) and the odds of small- or large-for-gestational age (SGA and LGA) births.Methods: This case-control study was comprised of SGA (N = 31), LGA (N = 28), and appropriate for gestational age control (N = 31) births selected from the larger LIFECODES cohort. Biomarkers of exposure to consumer product chemicals were quantified in maternal urine collected from up to three study visits during pregnancy. In a single-pollutant approach, odds ratios (OR) and 95% confidence intervals (CI) of SGA and LGA associated with an interquartile range (IQR)-increase in exposure biomarkers were estimated using multinomial logistic regression. In a multi-pollutant approach, quantile g-computation was used to jointly estimate the OR (95% CI) of SGA and LGA per simultaneous one quartile-change in all biomarkers belonging to each chemical class. Results: Among the 33 biomarkers analyzed, 20 were detected in at least 50% of the participants. After adjusting for potential confounders, we observed reduced odds of LGA in association with higher urinary concentrations of several exposure biomarkers. For example, an IQR-increase in the OPE metabolite, diphenyl phosphate, was associated with lower odds of LGA births (OR: 0.40 [95% CI: 0.18, 0.87]). Using quantile g-computation, we estimated lower odds of an LGA birth for higher OPE metabolite concentrations (OR: 0.49 [95% CI: 0.27, 0.89]) and phthalate metabolite concentrations (OR: 0.23 [95% CI: 0.07, 0.73]). Associations between consumer product chemicals and SGA were largely null. Conclusions: Joint exposure to OPEs and phthalates was associated with lower odds of delivering LGA. Associations with LGA could indicate a specific impact of these exposures on the high end of the birth weight spectrum. Future work to understand this nuance in the associations between consumer product chemical mixtures and fetal growth is warranted.

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Prenatal exposure to consumer product chemical mixtures and size for gestational age at delivery

10.21203/rs.3.rs-47532/v1 ◽

2020 ◽

Author(s):

Paige A Bommarito ◽

Barrett M. Welch ◽

Alexander P Keil ◽

George P Baker ◽

Dave E Cantonwine ◽

...

Keyword(s):

Prenatal Exposure ◽

Fetal Growth ◽

Gestational Age ◽

Multinomial Logistic Regression ◽

Consumer Products ◽

Consumer Product ◽

Chemical Mixtures ◽

Phthalate Metabolites ◽

Lower Odds ◽

Exposure Biomarkers

Abstract Background While fetal growth is a tightly regulated process, it is sensitive to environmental exposures that occur during pregnancy. Many commonly used consumer products contain chemicals that can disturb processes underlying fetal growth. However, mixtures of these chemicals have been minimally examined. We investigated associations between prenatal exposure to 33 consumer product chemicals (nine organophosphate ester flame retardant [OPE] metabolites, 12 phthalate metabolites, and 12 phenols) and the odds of small- or large-for-gestational age (SGA and LGA) births. Methods This case-control study was comprised of SGA (N = 31), LGA (N = 28), and appropriate for gestational age control (N = 31) births selected from the larger LIFECODES cohort. Biomarkers of exposure to consumer product chemicals were quantified in maternal urine collected from up to three study visits during pregnancy. In a single-pollutant approach, odds ratios (OR) and 95% confidence intervals (CI) of SGA and LGA associated with an interquartile range (IQR)-increase in exposure biomarkers were estimated using multinomial logistic regression. In a multi-pollutant approach, quantile g-computation was used to jointly estimate the OR (95% CI) of SGA and LGA per simultaneous one quartile-change in all biomarkers belonging to each chemical class. Results Among the 33 biomarkers analyzed, 20 were detected in at least 50% of the participants. After adjusting for potential confounders, we observed reduced odds of LGA in association with higher urinary concentrations of several exposure biomarkers. For example, an IQR-increase in the OPE metabolite, diphenyl phosphate, was associated with lower odds of LGA births (OR: 0.40 [95% CI: 0.18, 0.87]). Using quantile g-computation, we estimated lower odds of an LGA birth for lower OPE metabolites (OR: 0.49 [95% CI: 0.27, 0.89]) and phthalate metabolites (OR: 0.23 [95% CI: 0.07, 0.73]). Associations between consumer product chemicals and SGA were largely null. Conclusions Joint exposure to OPEs and phthalates was associated with lower odds of delivering LGA. Associations with LGA could indicate a specific impact of these exposures on the high end of the birth weight spectrum. Future work to understand this nuance in the associations between consumer product chemical mixtures and fetal growth is warranted.

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Sex-specific associations of prenatal exposure to bisphenol A and its alternatives with fetal growth parameters and gestational age

Environment International ◽

10.1016/j.envint.2020.106305 ◽

2021 ◽

Vol 146 ◽

pp. 106305

Author(s):

Pan Yang ◽

Bi-Gui Lin ◽

Bin Zhou ◽

Wen-Cheng Cao ◽

Pan-Pan Chen ◽

...

Keyword(s):

Bisphenol A ◽

Prenatal Exposure ◽

Fetal Growth ◽

Gestational Age ◽

Growth Parameters

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Prenatal Exposure to Nonpersistent Chemical Mixtures and Fetal Growth: A Population-Based Study

Environmental Health Perspectives ◽

10.1289/ehp9178 ◽

2021 ◽

Vol 129 (11) ◽

Author(s):

Michiel A. van den Dries ◽

Alexander P. Keil ◽

Henning Tiemeier ◽

Anjoeka Pronk ◽

Suzanne Spaan ◽

...

Keyword(s):

Prenatal Exposure ◽

Fetal Growth ◽

Population Based ◽

Chemical Mixtures ◽

Population Based Study

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Effects of prenatal exposure factors on birth outcomes through mediation of favorable fetal growth conditions using structural equation modeling

PLoS ONE ◽

10.1371/journal.pone.0249664 ◽

2021 ◽

Vol 16 (4) ◽

pp. e0249664

Author(s):

Aweke A. Mitku ◽

Temesgen Zewotir ◽

Delia North ◽

Prakash Jeena ◽

Rajen N. Naidoo

Keyword(s):

Risk Factors ◽

Weight Gain ◽

Gestational Weight Gain ◽

Birth Outcomes ◽

Prenatal Exposure ◽

Fetal Growth ◽

Gestational Age ◽

Structural Equation ◽

Growth Conditions ◽

Gestational Weight

Background Birth weight, birth length, and gestational age are major indicators of newborn health. Several prenatal exposure factors influence the fetal environment. The aim of the study was to investigate the effect of prenatal exposure factors, including socio-demographic, behavioural, dietary, physical activity, clinical and environmental on birth outcomes through the mediation of Favourable Fetal Growth Conditions (FFGC). Methods Data was obtained from six hundred and fifty-six Mother and Child in the Environment birth cohort study in Durban, South Africa from 2013 to 2017. We adopted structural equation models which evaluate the direct and indirect effects by allowing multiple simultaneous equations to incorporate confounding and mediation. Results A significant direct and indirect effect of FFGC on newborn weight, length, and gestational age was seen. Gestational weight gain and maternal body mass index in the first trimester exerted a mediation effect between maternal behavioural risk factors and FFGC. Similarly, the level of physical activity during pregnancy was associated with decreased gestational weight gain. The effects of maternal characteristics on newborn weight, length, and gestational age were largely indirect, operating through FFGC as a latent variable. Conclusions Gestational weight gain and maternal pre-gestational BMI were observed to mediate the association between prenatal behavioural risk factors and favourable fetal growth conditions. Trial registration Retrospectively registered from 01 March 2013.

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Modulation of birthweight through gestational age and fetal growth

Child Care Health and Development ◽

10.1046/j.1365-2214.1996.773773.x ◽

1996 ◽

Vol 22 (1) ◽

pp. 37-53 ◽

Cited By ~ 1

Author(s):

E Petridou ◽

D Trichopoulos ◽

K Revinthi ◽

D Tong ◽

E Papathoma

Keyword(s):

Fetal Growth ◽

Gestational Age

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INTRAUTERINE GROWTH RETARDATION - A REVIEW ARTICLE

Journal of Medicine and Pharmacy ◽

10.34071/jmp.2018.6.25a ◽

2018 ◽

pp. 184-195

Author(s):

Minh Son Pham ◽

Vu Quoc Huy Nguyen ◽

Dinh Vinh Tran

Keyword(s):

Fetal Growth ◽

Gestational Age ◽

Small For Gestational Age ◽

Fetal Growth Restriction ◽

Growth Restriction ◽

Growth Potential ◽

National Guidelines ◽

Intrauterine Growth ◽

No Gold Standard

Small for gestational age (SGA) and fetal growth restriction (FGR) is difficult to define exactly. In this pregnancy condition, the fetus does not reach its biological growth potential as a consequence of impaired placental function, which may be because of a variety of factors. Fetuses with FGR are at risk for perinatal morbidity and mortality, and poor long-term health outcomes, such as impaired neurological and cognitive development, and cardiovascular and endocrine diseases in adulthood. At present no gold standard for the diagnosis of SGA/FGR exists. The first aim of this review is to: summarize areas of consensus and controversy between recently published national guidelines on small for gestational age or fetal growth restriction; highlight any recent evidence that should be incorporated into existing guidelines. Another aim to summary a number of interventions which are being developed or coming through to clinical trial in an attempt to improve fetal growth in placental insufficiency. Key words: fetal growth restriction (FGR), Small for gestational age (SGA)

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