Evidence map›Paper›PMID 23299301›Full record

ArticleJournal of exposure science & environmental epidemiology2013

The relationship between prenatal exposure to airborne polycyclic aromatic hydrocarbons (PAHs) and PAH-DNA adducts in cord blood.

Wieslaw A Jedrychowski, Frederica P Perera, Deliang Tang, Virginia Rauh, Renata Majewska, Elzbieta Mroz, Elzbieta Flak, Laura Stigter, John Spengler, David Camann and 1 more

Abstract read
In one paragraph

Article in Journal of exposure science & environmental epidemiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

19 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Biomarkers used in studying air pollution exposure during pregnancy and perinatal outcomes: a review.Biomarkers : biochemical indicators of exposure, response, and susceptibility to chemicals · 2017
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Prenatal protection: maternal diet may modify impact of PAHs.Environmental health perspectives · 2013
    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

11 authors.

Wieslaw A JedrychowskiDepartment of Epidemiology and Preventive Medicine, Jagiellonian University Medical College, Krakow, Poland. myjedryc@cyf-kr.edu.pl
Frederica P Perera
Deliang Tang
Virginia Rauh
Renata Majewska
Elzbieta Mroz
Elzbieta Flak
Laura Stigter
John Spengler
David Camann
Ryszard Jacek

Funding

VULNERABILITY OF THE FETUS/INFANT TO PAH, PM2.5 AND ETS.R01ES010165 · NIEHS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI PERERA, FREDERICA P · 2000 to 2004
$3.2M
NIEHS NIH HHS 5 R01 ES10165NIEHS NIH HHS R01 ES010165NIEHS NIH HHS R01 ES010165-0451
6 · The paper itself

Abstract

In a birth cohort study, we have assessed the dose-response relationship between individual measurements of prenatal airborne polycyclic aromatic hydrocarbon (PAH) exposure and specific PAH-DNA adducts in cord blood adjusted for maternal blood adducts and season of birth. The study uses data from an earlier established birth cohort of children in Krakow. The final analysis included 362 pregnant women who gave birth to term babies and had complete data on personal exposure in the second trimester of pregnancy to eight airborne PAHs including benzo[a]pyrene (B[a]P), as well as DNA adducts, both in maternal and cord blood. The relation between cord blood PAH-DNA adducts and airborne prenatal PAH exposure was non-linear. Although cord blood PAH-DNA adducts were significantly associated with the B[a]P exposure categorized by tertiles (non-parametric trend z=3.50, P<0.001), the relationship between B[a]P and maternal blood adducts was insignificant (z=1.63, P=0.103). Based on the multivariable linear regression model, we estimated the effect of the prenatal airborne B[a]P on the level of cord blood adducts. In total, 14.8% of cord blood adducts variance was attributed to the level of maternal adducts and 3% to a higher prenatal B[a] exposure above 5.70 ng/m(3). The calculated fetal/maternal blood adduct ratio (FMR) linearly increased with B[a]P exposure (z=1.99, P=0.047) and was highest at B[a]P concentrations exceeding 5.70 ng/m(3). In conclusion, the results support other findings that transplacental exposure to B[a]P from maternal inhalation produces DNA damage in the developing fetus. It also confirms the heightened fetal susceptibility to prenatal PAH exposure that should be a matter of public health concern, particularly in the highly polluted areas, because DNA adducts represent a pro-carcinogenic alteration in DNA. The continuation of this birth cohort study will assess the possible health effects of fetal DNA damage on the health of children and help in establishing new protective guidelines for newborns.

Indexed as

AdolescentAdultDNA AdductsFemaleFetal BloodHumansInhalation ExposureMaleParticulate MatterPolycyclic Aromatic HydrocarbonsPregnancyYoung AdultDNA AdductsParticulate MatterPolycyclic Aromatic Hydrocarbons

Identifiers

PMID23299301
PMCPMC3733112

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.