Evidence map›Paper›PMID 14754571›Full record

ArticleEnvironmental health perspectives2004

Developmental effects of chlorpyrifos extend beyond neurotoxicity: critical periods for immediate and delayed-onset effects on cardiac and hepatic cell signaling.

Armando Meyer, Frederic J Seidler, Theodore A Slotkin

Open access · diamondAbstract read
In one paragraph

Article in Environmental health perspectives, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
6.7field-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

30 citing papers in PubMed, 62 citations in OpenAlex.

  1. Chlorpyrifos and Chlorpyrifos-Oxon: A Widening Spectrum of Toxicity.International journal of molecular sciences · 2026
    Review
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  11. Induction of endocannabinoid levels in juvenile rat brain following developmental chlorpyrifos exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2013
    Article
  12. Article
  13. Effect of developmental chlorpyrifos exposure, on endocannabinoid metabolizing enzymes, in the brain of juvenile rats.Toxicological sciences : an official journal of the Society of Toxicology · 2011
    Article
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  15. Review
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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

3 authors at 1 institution in 1 country.

Armando MeyerCentro de Estudos da Saúde do Trabalhador e Ecologia Humana, Escola Nacional de Saúde Pública, Fundação Oswaldo Cruz, Rio de Janeiro, Brazil.
Frederic J Seidler
Theodore A Slotkin
Escola Nacional de Saúde Pública · BR

Funding

Zebrafish as a Detector of Organophosphate ExposureP42ES010356 · NIEHS · DUKE UNIVERSITY · PI EDWARD D LEVIN · 2000 to 2026
$56.2M
MECHANISMS OF CHLORPYRIFOS DEVELOPMENTAL NEUROTOXICITYR01ES010387 · NIEHS · DUKE UNIVERSITY · PI SLOTKIN, THEODORE A · 2000 to 2004
$963k
NIEHS NIH HHS ES10356NIEHS NIH HHS ES10387
6 · The paper itself

Abstract

The fetal and neonatal neurotoxicity of chlorpyrifos (CPF) and related insecticides is a major concern. Developmental effects of CPF involve mechanisms over and above cholinesterase inhibition, notably events in cell signaling that are shared by nonneural targets. In the present study, we evaluated the immediate and long-term effects of CPF exposure of rats during different developmental windows [gestational days (GD) 9-12 or 17-20, postnatal days (PN) 1-4 or 11-14] on the adenylyl cyclase (AC) signaling cascade in the heart and liver. In addition to basal AC activity, we assessed the responses to direct AC stimulants (forskolin, Mn2+); to isoproterenol and glucagon, which activate signaling through specific membrane receptors; and to sodium fluoride, which activates the G-proteins that couple the receptors to AC. Few immediate effects on AC were apparent when CPF doses remained below the threshold for systemic toxicity. Nevertheless, CPF exposures on GD9-12, GD17-20, or PN1-4 elicited sex-selective effects that emerged by adulthood (PN60), whereas later exposure (PN11-14) elicited smaller, nonsignificant effects, indicative of closure of the window of vulnerability. Most of the effects were heterologous, involving signaling elements downstream from the receptors, and thus were shared by multiple inputs; superimposed on this basic pattern, there were also selective alterations in receptor-mediated responses. These results suggest that the developmental toxicity of CPF extends beyond the nervous system, to include cell signaling cascades that are vital to cardiac and hepatic homeostasis. Future work needs to address the potential implications of these effects for cardiovascular and metabolic disorders that may emerge long after the end of CPF exposure.

Indexed as

Prenatal Exposure Delayed EffectsAdenylyl CyclasesAnimalsChlorpyrifosFemaleHeartHomeostasisInsecticidesLiverMyocardiumPregnancyRatsRats, Sprague-DawleySignal TransductionAdenylyl CyclasesChlorpyrifosInsecticides

Identifiers

PMID14754571
PMCPMC1241826
OpenAlexW2021840572

What OpenQuestion holds

Textmetadata
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.