Prenatal lead exposure, telomere length in cord blood, and DNA methylation age in the PROGRESS prenatal cohort

Herrera-Moreno, José Francisco; Estrada-Gutiérrez, Guadalupe; Wu, Haotian; Bloomquist, Tessa R.; Rosa, Maria José; Just, Allan C.; Lamadrid-Figueroa, Héctor; Téllez‐Rojo, Martha María; Wright, Robert O.; Baccarelli, Andrea A.

doi:10.1016/j.envres.2021.112577

Cited by 12 publications

(4 citation statements)

References 85 publications

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“…Neighbourhood level toxicant and pollutant-related exposures (e.g., PM 2.5 , Ozone, proximity to Superfund sites) were not associated with gestational epigenetic age signatures in this study. This was somewhat surprising given some other studies have found that prenatal exposure to metals, air pollutants, and other environmental risks are associated with DNA methylation at birth [ 52–55 ], though studies of gestational epigenetic age acceleration and prenatal toxicant exposure are fewer and have not been as consistent [ 56 , 57 ]. In our study, we relied on the COI to index area-based toxicant exposure.…”

Section: Discussionmentioning

confidence: 99%

Maternal depression and adverse neighbourhood conditions during pregnancy are associated with gestational epigenetic age deceleration

et al. 2022

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Gestational epigenetic age (GEA) acceleration and deceleration can indicate developmental risk and may help elucidate how prenatal exposures lead to offspring outcomes. Depression and neighbourhood conditions during pregnancy are well-established determinants of birth and child outcomes. Emerging research suggests that maternal depression may contribute to GEA deceleration. It is unknown whether prenatal neighbourhood adversity would likewise influence GEA deceleration. This study examined whether maternal depression and neighbourhood conditions independently or jointly contributed to GEA deceleration, and which social and environmental neighbourhood conditions were associated with GEA. Participants were from the Albany Infant and Mother Study (n = 204), a prospective non-probability sampled cohort of higher risk racial/ethnic diverse mother/infant dyads. GEA was estimated from cord blood. Depressive symptoms and census-tract level neighbourhood conditions were assessed during pregnancy. Maternal depression (β = −0.03, SE = 0.01, p = 0.008) and neighbourhood adversity (β = −0.32, SE = 0.14, p = 0.02) were independently associated with GEA deceleration, controlling for all covariates including antidepressant use and cell type proportions. Neighbourhood adversity did not modify the association of maternal depression and GEA (β = 0.003, SE = 0.03, p = 0.92). igher levels of neighbourhood poverty, public assistance, and lack of healthy food access were each associated with GEA deceleration; higher elementary school test scores (an indicator of community tax base) were associated with GEA acceleration (all p < 0.001). The results of this study indicated that maternal depression and neighbourhood conditions were independently and cumulatively associated GEA in this diverse population.

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Section: Discussionmentioning

confidence: 99%

Maternal depression and adverse neighbourhood conditions during pregnancy are associated with gestational epigenetic age deceleration

et al. 2022

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“…There is evidence that long-term chronic lead exposure is associated with abnormal DNA methylation in children, and this DNA methylation may mediate lead-related myocardial damage, which may genetically affect the occurrence of SC-MI (42)(43)(44)(45). Nevertheless, more basic and clinical studies are needed to explore proven and potential mechanisms.…”

Section: Figurementioning

confidence: 99%

Lead exposure is non-linearly associated with subclinical myocardial injury in the general population without cardiovascular disease

Wang

Huang²,

Li³

et al. 2022

Front. Public Health

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Background and aimsGrowing studies have focused on the effect of lead exposure on human circulatory system, while the relationship between lead exposure and subclinical myocardial injury (SC-MI) is still poorly known. Therefore, this study was to explore the effect of lead exposure on SC-MI.MethodsThe study included 6,272 individuals aged 40 and older without cardiovascular disease (CVD) from the third National Health and Nutrition Examination Survey. Blood lead was used as an alternative marker of lead exposure. Multivariable logistic regression models, restricted cubic spline and threshold effect analyses were performed to investigate the effect of blood lead on SC-MI.ResultsAfter adjusting for age, sex, race, diabetes, hypertension, systolic blood pressure, body mass index, waist-to-hip ratio, triglycerides, total cholesterol, creatinine, fasting plasma glucose and hemoglobin Alc, higher blood lead level was independently related to higher risk of SC-MI (OR 1.047, 95% CI [1.018, 1.077]; P = 0.003). Restricted cubic spline curve showed that there was a non-linear correlation between blood lead and SC-MI. Threshold effect analysis determined that the inflection point of blood lead was 3.8 ug/dl. When the blood lead level was higher than 3.8 ug/dl, there was an independent positive correlation between blood lead level and the risk of SC-MI (OR 1.031, 95% CI [1.009, 1.053]; P < 0.01). And similar associations were also observed among subgroups of male, ≤60 years, >60 years, never smoker, non-Hispanic White, non-Hispanic Black or without hypertension and diabetes.ConclusionsBlood lead was non-linearly related to SC-MI in population free from CVD.

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“…Specifically, the researchers investigated the relationship between intrauterine fetal Pb exposure, telomere length, and epigenetic aging trends (Horvath’s DNA methylation age and Knight’s predictor of gestational age) through analysis of cord blood (leukocyte) samples and postnatal bone Pb levels. No significant associations were found between these data and Pb levels in children’s bones, pointing out no consequences at the level of epigenetic aging for infants exposed intrauterinally to Pb [ 119 ].…”

Section: Link Between Toxicants Exposure Dna Methylation and Survivalmentioning

confidence: 99%

Evolutionary Implications of Environmental Toxicant Exposure

et al. 2022

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Homo sapiens have been exposed to various toxins and harmful compounds that change according to various phases of human evolution. Population genetics studies showed that such exposures lead to adaptive genetic changes; while observing present exposures to different toxicants, the first molecular mechanism that confers plasticity is epigenetic remodeling and, in particular, DNA methylation variation, a molecular mechanism proposed for medium-term adaptation. A large amount of scientific literature from clinical and medical studies revealed the high impact of such exposure on human biology; thus, in this review, we examine and infer the impact that different environmental toxicants may have in shaping human evolution. We first describe how environmental toxicants shape natural human variation in terms of genetic and epigenetic diversity, and then we describe how DNA methylation may influence mutation rate and, thus, genetic variability. We describe the impact of these substances on biological fitness in terms of reproduction and survival, and in conclusion, we focus on their effect on brain evolution and physiology.

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Prenatal lead exposure, telomere length in cord blood, and DNA methylation age in the PROGRESS prenatal cohort

Cited by 12 publications

References 85 publications

Maternal depression and adverse neighbourhood conditions during pregnancy are associated with gestational epigenetic age deceleration

Maternal depression and adverse neighbourhood conditions during pregnancy are associated with gestational epigenetic age deceleration

Lead exposure is non-linearly associated with subclinical myocardial injury in the general population without cardiovascular disease

Evolutionary Implications of Environmental Toxicant Exposure

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