Prenatal exposure to polycyclic aromatic hydrocarbons and gestational age at birth

Freije, Sophia L.; Enquobahrie, Daniel A.; Day, Drew B; Loftus, Christine T.; Szpiro, Adam A.; Karr, Catherine J.; Trasande, Leonardo; Kahn, Linda G.; Barrett, Emily S.; Kannan, Kurunthachalam; Bush, Nicole R.; LeWinn, Kaja Z.; Swan, Shanna H.; Mason, W. Alex; Robinson, Morgan; Sathyanarayana, Sheela

doi:10.1016/j.envint.2022.107246

Cited by 19 publications

(13 citation statements)

References 67 publications

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“…However, the association did not hold for later preterm deliveries and, in some models examining other exposure windows, associations appeared to be protective. Most recently, we analyzed harmonized data from CANDLE and two additional cohorts, observing that 10-fold higher second trimester 2-OH-NAP concentrations were associated with 1.6 day shorter gestation, with some evidence of greater vulnerability to spontaneous preterm birth among female fetuses (19). In the current analysis associations between 2-OH-NAP and pCRH were weak and included the null.…”

Section: Discussionmentioning

confidence: 89%

“…The widespread PAH exposure documented in pregnant people is of particular concern given fetal vulnerability to environmental contaminants, including endocrine disruptors (18). Recent work from our group examined urinary hydroxylated PAH metabolites (OH-PAHs), a common biomarker of PAH exposure, reporting that higher second trimester urinary 2-hydroxynaphthalene (2-OH-NAP) was associated with earlier gestational age at birth and higher 1hydroxypyrene (1-OH-PYR) with increased odds of spontaneous preterm birth among participants carrying female infants (19). Several studies examining alternative measures of PAH exposure, such PAH-DNA adducts and air monitoring, have similarly reported associations with shorter gestation (20) and increased risk of preterm birth (21,22).…”

Section: Introductionmentioning

confidence: 99%

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Prenatal polycyclic aromatic hydrocarbon (PAH) exposure in relation to placental corticotropin releasing hormone (pCRH) in the CANDLE pregnancy cohort

Barrett

Workman²,

Hazlehurst³

et al. 2022

Front. Endocrinol.

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Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous endocrine-disrupting combustion by-products that have been linked to preterm birth. One possible mechanism is through disruption of placental corticotropin releasing hormone (pCRH), a key hormone implicated in parturition. As an extension of recent research identifying pCRH as a potential target of endocrine disruption, we examined maternal PAH exposure in relation to pCRH in a large, diverse sample. Participants, drawn from the CANDLE cohort, part of the ECHO-PATHWAYS Consortium, completed study visits at 16-29 weeks (V1) and 22-39 weeks (V2) gestation (n=812). Seven urinary mono-hydroxylated PAH metabolites (OH-PAHs) were measured at V1 and serum pCRH at V1 and V2. Associations between individual log-transformed OH-PAHs (as well as two summed PAH measures) and log(pCRH) concentrations across visits were estimated using mixed effects models. Minimally-adjusted models included gestational age and urinary specific gravity, while fully-adjusted models also included sociodemographic characteristics. We additionally evaluated effect modification by pregnancy complications, fetal sex, and maternal childhood trauma history. We observed associations between 2-OH-Phenanthrene (2-OH-PHEN) and rate of pCRH change that persisted in fully adjusted models (β=0.0009, 0.00006, 0.0017), however, positive associations with other metabolites (most notably 3-OH-Phenanthrene and 1-Hydroxypyrene) were attenuated after adjustment for sociodemographic characteristics. Associations tended to be stronger at V1 compared to V2 and we observed no evidence of effect modification by pregnancy complications, fetal sex, or maternal childhood trauma history. In conclusion, we observed modest evidence of association between OH-PAHs, most notably 2-OH-PHEN, and pCRH in this sample. Additional research using serial measures of PAH exposure is warranted, as is investigation of alternative mechanisms that may link PAHs and timing of birth, such as inflammatory, epigenetic, or oxidative stress pathways.

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Section: Discussionmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Prenatal polycyclic aromatic hydrocarbon (PAH) exposure in relation to placental corticotropin releasing hormone (pCRH) in the CANDLE pregnancy cohort

Barrett

Workman²,

Hazlehurst³

et al. 2022

Front. Endocrinol.

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“…Prenatal exposures to PAHs have been linked to adverse birth outcomes such as fetal growth restriction and preterm birth [6,7]. They have also been related to neurodevelopment [8] and childhood asthma [9], yet the biological mechanisms through which PAHs exhibit such toxicity are still debated.…”

Section: Discussionmentioning

confidence: 99%

Urinary polycyclic aromatic hydrocarbon metabolites and their association with oxidative stress among pregnant women in Los Angeles

Meng,

Mitra,

Rosario

et al. 2024

Preprint

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Background Polycyclic aromatic hydrocarbons (PAHs) have been linked to adverse birth outcomes, but few epidemiological studies to date have evaluated associations between urinary PAH metabolites and oxidative stress biomarkers in pregnancy. Methods We measured a total of 7 PAH metabolites and 2 oxidative stress biomarkers (malondialdehyde (MDA), 8-hydroxy-2’-deoxyguanosine (8-OHdG)) in urine samples collected up to three times during pregnancy in 159 women enrolled at antenatal clinics at the University of California Los Angeles during 2016–2019. Using multiple linear regression models, we estimated the percentage change (%) and 95% confidence interval (CI) in 8-OHdG and MDA measured at each sample collection time per doubling of PAH metabolite concentrations. Results Most PAH metabolites were positively associated with both urinary oxidative stress biomarkers, MDA and 8-OHdG, with stronger associations in early and late pregnancy. Women pregnant with male fetuses exhibited slightly larger increases in both MDA and 8-OHdG in association with PAH exposures in early and late pregnancy. Conclusion Urinary OH-PAH biomarkers are associated with increases in oxidative stress during pregnancy, especially in early and late pregnancy. Sex differences in associations between PAH exposures and oxidative stress need to be further explored in the future.

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“…There is strong evidence indicating that prenatal exposure to PM 2.5 , PM 1 , PM 10 or PM 2.5 constituents increases the risk of PTB [ 39 , 40 , 41 , 42 , 43 , 44 ]. Studies have also reported that CO and PAHs are potential risk factors for PTB [ 45 , 46 , 47 ]. Building upon the speculations from these previous studies, this study hypothesized that prenatal exposure to MCS might result in a significantly higher risk of PTB.…”

Section: Discussionmentioning

confidence: 99%

First Trimester of Pregnancy as the Sensitive Period for the Association between Prenatal Mosquito Coil Smoke Exposure and Preterm Birth

Liu

Strodl

et al. 2022

IJERPH

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Mosquito coils are efficient mosquito repellents and mosquito coil smoke (MCS) contributes to indoor air pollution. However, no prior population-based study has investigated whether prenatal MCS exposure is a risk factor for preterm birth (PTB) and whether exposure to MCS in different trimesters of pregnancy is associated with different levels of risk. The sample involved 66,503 mother–child dyads. Logistic regression models were used to examine the relationships between prenatal MCS exposure during different trimesters of pregnancy and PTB. We found that prenatal MCS exposure was associated with a greater likelihood of PTB (OR = 1.12, 95%CI: 1.05–1.20). The prenatal MCS exposure during the first trimester was associated with 1.17 (95%CI: 1.09–1.25) times the odds of being PTB, which was higher than exposure during the second trimester (OR = 1.11, 95%CI: 1.03–1.19) and during the third trimester (OR = 1.08, 95%CI: 1.01–1.16). In the stratified analysis, prenatal MCS exposure significantly increased PTB risk among girls but not among boys. Our results indicated that maternal MCS exposure during pregnancy was associated with PTB and that the first trimester might be the sensitive period. In light of these findings, public health interventions are needed to reduce prenatal exposure to MCS, particularly during the first trimester of pregnancy.

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Prenatal exposure to polycyclic aromatic hydrocarbons and gestational age at birth

Cited by 19 publications

References 67 publications

Prenatal polycyclic aromatic hydrocarbon (PAH) exposure in relation to placental corticotropin releasing hormone (pCRH) in the CANDLE pregnancy cohort

Prenatal polycyclic aromatic hydrocarbon (PAH) exposure in relation to placental corticotropin releasing hormone (pCRH) in the CANDLE pregnancy cohort

Urinary polycyclic aromatic hydrocarbon metabolites and their association with oxidative stress among pregnant women in Los Angeles

First Trimester of Pregnancy as the Sensitive Period for the Association between Prenatal Mosquito Coil Smoke Exposure and Preterm Birth

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