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Long-term Behavioral and Reproductive Consequences of Embryonic Exposure to Low-dose Toxicants
Published on: March 6, 2018
Associations between gestational polybrominated diphenyl ether (PBDE) serum concentrations and child sleep outcomes
Kelli Williams1, Jagadeesh Puvvula1, John H Holmes1
1Department of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, 19104, United States.
Insights
Gestational exposure to polybrominated diphenyl ethers (PBDEs) is linked to increased sleep irregularity and disruption in children. This research highlights potential sleep disruptions as a factor in PBDE-associated neurobehavioral issues.
Area of Science:
- Environmental Health
- Pediatric Sleep Medicine
- Toxicology
Background:
- Gestational exposure to polybrominated diphenyl ethers (PBDEs) is a known endocrine disruptor, linked to thyroid issues in mothers and neurobehavioral effects in children.
- The impact of prenatal PBDE exposure on children's sleep patterns remains largely uncharacterized.
Purpose of the Study:
- To investigate the association between gestational exposure to specific PBDE congeners and various sleep parameters in children from ages 2 to 8 years.
- To explore the longitudinal relationship between prenatal PBDE levels and child sleep irregularity, hypersomnolence, sleep disruption, and sleep duration.
Main Methods:
- Utilized data from 410 mother-child dyads in the Health Outcomes and Measures of the Environment (HOME) Study.
- Measured gestational serum PBDE levels (including PBDE-153, -100, -99, -47, -28, and ΣPBDEs) and child sleep patterns via the adapted Child Sleep Health Questionnaire.
- Employed generalized estimating equations to assess longitudinal associations, adjusting for relevant covariates.
Main Results:
- Gestational PBDE-99, PBDE-47, and ΣPBDEs were associated with increased sleep irregularity across all observed years.
- PBDE-28 exposure was linked to higher sleep irregularity at ages 5 and 8 years.
- PBDE-47, PBDE-99, and ΣPBDEs showed associations with increased sleep disruption in children over time.
- No significant associations were found between gestational PBDEs and children's sleep duration.
Conclusions:
- Prenatal exposure to certain PBDEs is associated with sleep irregularity and disruption in children.
- Sleep disturbances may serve as a crucial mediator in the neurobehavioral effects linked to gestational PBDE exposure.
- Further research is warranted to understand the mechanisms and implications of these findings for child development.
Abstract:
Gestational polybrominated diphenyl ethers (PBDEs) exposures have been associated with thyroid disruption in pregnant women and adverse neurobehavioral outcomes in their children, but it is unknown if they interfere with children's sleep patterns. We assessed gestational PBDE exposure (16 weeks) and child sleep patterns from ages 2-8 years using 410 mother-child dyads in the Health Outcomes and Measures of the Environment (HOME) Study. Gestational biomarkers of serum PBDEs include PBDE-153 (GM ± GSD: 5.2 ± 2.8 ng/g lipid), PBDE-100 (4 ± 2.6), PBDE-99 (4.6 ± 2.7), PBDE-47 (20.2 ± 2.6), PBDE-28 (1.3 ± 2.2), and ΣPBDEs (37.03 ± 2.52). We measured child sleep patterns using the adapted Child Sleep Health Questionnaire, which includes sleep irregularity (mean ± SD: 2.5 ± 0.8), hypersomnolence (4.7 ± 1.5), sleep disruption (6.7 ± 1.6), and sleep duration. We assessed longitudinal associations between gestational PBDEs and sleep patterns using generalized estimating equations, adjusting for covariates. For PBDE-visit interactions (p < 0.1), visit-specific estimates with 95 % CIs were calculated; otherwise, the overall estimate was reported. Every 10-fold increase in PBDE-99 (β = 0.18, 95 % CI: 0.04, 0.23), PBDE-47 (0.15, 95 % CI: 0.001, 0.3) and ΣPBDEs (0.13, 95 % CI: 0.21, 0.27) was associated with increased sleep irregularity for all years, and PBDE-28 was associated with this outcome at age 5 and 8 years (0.43, 95 % CI: 0.09, 0.77). PBDE-153 (-0.5, 95 % CI: 1.06, 0.05) was associated with decreased hypersomnolence at age 4 years. PBDE-47 (0.3, 95 % CI: 0.004, 0.61), PBDE-99 (0.38, 95 % CI: 0.1, 0.67 and 0.62), and ΣPBDEs (0.27, 95 % CI: 0.02, 0.56) were associated with increased sleep disruption for all ages. We observed no significant associations between PBDEs and sleep duration. We found that gestational PBDEs were associated with sleep irregularity and sleep disruption in children, highlighting the need to explore sleep as a mediator of PBDE-associated neurobehavioral problems.
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