2017 Study Abstract
Background
Adverse effects of prenatal stress or environmental chemical exposures on fetal growth are well described, yet their combined effect remains unclear.
Objectives
To conduct a systematic review on the combined impact and interaction of prenatal exposure to stress and chemicals on developmental outcomes.
Methods
We used the first three steps of the Navigation Guide systematic review. We wrote a protocol, performed a robust literature search to identify relevant animal and human studies and extracted data on developmental outcomes. For the most common outcome (fetal growth), we evaluated risk of bias, calculated effect sizes for main effects of individual and combined exposures, and performed a random effects meta-analysis of those studies reporting on odds of low birthweight (LBW) by smoking and socioeconomic status (SES).
Results
We identified 17 human- and 22 animal-studies of combined chemical and stress exposures and fetal growth. Human studies tended to have a lower risk of bias across nine domains. Generally, we found stronger effects for chemicals than stress, and these exposures were associated with reduced fetal growth in the low-stress group and the association was often greater in high stress groups, with limited evidence of effect modification. We found smoking associated with significantly increased odds of LBW, with a greater effect for high stress (low SES; OR 4.75 (2.46–9.16)) compared to low stress (high SES; OR 1.95 (95% CI 1.53–2.48)). Animal studies generally had a high risk of bias with no significant combined effect or effect modification.
Conclusions
We found that despite concern for the combined effects of environmental chemicals and stress, this is still an under-studied topic, though limited available human studies indicate chemical exposures exert stronger effects than stress, and this effect is generally larger in the presence of stress.
Sources
- Cumulative effects of prenatal-exposure to exogenous chemicals and psychosocial stress on fetal growth: Systematic-review of the human and animal evidence, PLOS one doi.org/10.1371/journal.pone.0176331, July 12, 2017.
- DES studies on fertility and pregnancy.
- Feature image credit @ToxicsFree
I have expressed this before but I am the product of embryonic intersex sexual development issues. It has been long suspected to the cause of my gender ambiguity was exposure to DED and or other form of EDC endocrine disrupter chemicals.
Corrective surgeries for me started at age ten and now I’m a much older adult and I’ll need several more surgeries to address these health issues.
The doctors I have learn to trust feel EDC were the cause of my intersex. Living in my small community I know others who have suffered the same as myself. Even my own spouse has DES exposure problems. In addition her older bother and two younger sisters.
Thank you once again Dave, for sharing your tragic experiences with our readers.
Best wishes,