Evidence map›Paper›PMID 38281572›Full record

SynthesisEnvironmental pollution (Barking, Essex : 1987)2024

Lead exposure, glucocorticoids, and physiological stress across the life course: A systematic review.

O M Halabicky, C W Giang, A L Miller, K E Peterson

Open access · greenAbstract readSystematic Review
In one paragraph

Synthesis in Environmental pollution (Barking, Essex : 1987), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 2 pooled it
4.7field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 2 syntheses or guidelines pooled it, 16 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

O M HalabickyDepartment of Nutritional Sciences, School of Public Health, University of Michigan, 1415 Washington Heights, Ann Arbor, MI, USA. Electronic address: oliviamh@umich.edu.
C W GiangDepartment of Health Behavior and Health Education, School of Public Health, University of Michigan, 1415 Washington Heights, Ann Arbor, MI, USA. Electronic address: cgaing@umich.edu.
A L MillerDepartment of Health Behavior and Health Education, School of Public Health, University of Michigan, 1415 Washington Heights, Ann Arbor, MI, USA. Electronic address: alimill@umich.edu.
K E PetersonDepartment of Nutritional Sciences, School of Public Health, University of Michigan, 1415 Washington Heights, Ann Arbor, MI, USA. Electronic address: karenep@umich.edu.
University of Michigan–Ann Arbor · US

Funding

ENVIRONMENTAL TOXICOLOGY PRE/POST DOCTORAL RES.TRAININGT32ES007062 · NIEHS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Justin Adam Colacino · 1985 to 2026
$10.5M
E3Gen: Multigenerational Influences of Social Structure on Toxicant Exposures and Life Course Health in the ELEMENT CohortR24ES028502 · NIEHS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Karen Eileen Peterson, Peter Xuekun Song · 2017 to 2026
$2.2M
NIEHS NIH HHS R24 ES028502NIEHS NIH HHS T32 ES007062
6 · The paper itself

Abstract

The biological pathways linking lead exposure to adverse outcomes are beginning to be understood. Rodent models suggest lead exposure induces dysfunction within the hypothalamic-pituitary-adrenal (HPA) axis and glucocorticoid regulation, a primary physiological stress response system. Over time, HPA axis and glucocorticoid dysfunction has been associated with adverse neurocognitive and cardiometabolic health, much like lead exposure. This systematic review utilized PRISMA guidelines to synthesize the literature regarding associations between lead exposure and downstream effector hormones of the HPA axis, including cortisol, a glucocorticoid, and dehydroepiandrosterone (DHEA), a glucocorticoid antagonist. We additionally determined the state of the evidence regarding lead exposure and allostatic load, a measure of cumulative body burden resultant of HPA axis and glucocorticoid dysfunction. A total of 18 articles were included in the review: 16 assessed cortisol or DHEA and 3 assessed allostatic load. Generally, the few available child studies suggest a significant association between early life lead exposure and altered cortisol, potentially suggesting the impact of developmental exposure. In adulthood, only cross sectional studies were available. These reported significant associations between lead and reduced cortisol awakening response and increased cortisol reactivity, but few associations with fasting serum cortisol. Two studies reported significant associations between increasing lead exposure and allostatic load in adults and another between early life lead exposure and adolescent allostatic load. The paucity of studies examining associations between lead exposure and allostatic load or DHEA and overall heterogeneity of allostatic load measurements limit conclusions. However, these findings cautiously suggest associations between lead and dysregulation of physiological stress pathways (i.e., glucocorticoids) as seen through cortisol measurement in children and adults. Future research would help to elucidate these associations and could further examine the physiological stress pathway as a mediator between lead exposure and detrimental health outcomes.

Indexed as

Environmental ExposureGlucocorticoidsHypothalamo-Hypophyseal SystemLeadPituitary-Adrenal SystemStress, PhysiologicalAdolescentChildDehydroepiandrosteroneEnvironmental PollutantsHumansHydrocortisoneDehydroepiandrosteroneEnvironmental PollutantsGlucocorticoidsHydrocortisoneLeadCortisolHPA axisLead exposureLife coursePhysiological stress systemsSystematic review

Identifiers

PMID38281572
PMCPMC12817149
OpenAlexW4391255515

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.