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Updated: Jun 10, 2026

Analysis of the Ambient Particulate Matter-induced Chromosomal Aberrations Using an In Vitro System
Published on: December 21, 2016
Prenatal PAH exposure is associated with chromosome-specific aberrations in cord blood
Manuela A Orjuela1, Xinhua Liu, Dorothy Warburton
1Departments of Pediatrics (Oncology) , Environmental Health Sciences, Biostatistics and Genetics, Columbia University, New York, NY, United States. is2148@columbia.edu
Insights
Prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) is linked to chromosomal aberrations in newborns, particularly in specific chromosomes. This association raises concerns about potential long-term cancer risks in children exposed to airborne PAHs.
Area of Science:
- Environmental Health
- Genetics
- Toxicology
Background:
- Chromosomal aberrations are established risk factors for adult cancers.
- Previous studies linked prenatal polycyclic aromatic hydrocarbon (PAH) exposure to chromosomal aberrations in cord blood.
- The chromosome-specific nature and extent of this association required further investigation.
Purpose of the Study:
- To determine if the association between airborne PAHs and chromosomal aberrations is chromosome-specific.
- To investigate if this association extends to smaller chromosomes.
- To assess the impact of prenatal PAH exposure on specific chromosome aberration frequencies.
Main Methods:
- Analysis of 48 cord blood samples from newborns with monitored prenatal airborne PAH exposure.
- Utilized whole chromosome paints for chromosomes 1-6, 11, 12, 14, 19, and a 6q sub-telomere probe.
- Scored 1500 metaphases per sample to calculate stable aberration frequencies and examined associations with PAH levels.
Main Results:
- Aberrations in chromosome 6 were more frequent than predicted by genomic content.
- Prenatal PAH levels and aberration frequencies in chromosomes 1-6 were halved compared to previous reports.
- Increased prenatal PAH exposure correlated with higher aberration frequencies in chromosomes 11-19 (p=0.02) and chromosome 6 (p=0.06), but not chromosomes 1-5.
Conclusions:
- Prenatal airborne PAH exposure is specifically associated with aberrations in chromosomes 6, 11, 12, 14, and 19.
- These chromosome-specific effects were observed even at lower airborne PAH levels.
- The findings raise concerns regarding the potential cancer risk associated with prenatal PAH exposure.
Abstract:
Chromosomal aberrations are associated with increased cancer risk in adults. Previously, we demonstrated that stable aberrations involving chromosomes 1-6 in cord blood are associated with prenatal exposure to polycyclic aromatic hydrocarbons (PAHs) measured in air and are disproportionate to genomic content. We now examine whether the association with air PAHs is chromosome-specific and extends to smaller chromosomes. Using whole chromosome paints for chromosomes 1-6, 11, 12, 14 and 19, and a 6q sub-telomere specific probe, we scored 48 cord bloods (1500 metaphases per sample) from newborns monitored prenatally for airborne PAH exposure in the Columbia Center for Children's Environmental Health cohort. Frequencies of stable aberrations were calculated as incident aberrations per 100 cell equivalents scored, and examined for association with airborne PAHs. Aberrations in chromosome 6 occurred more frequently than predicted by genomic content (p<0.008). Levels of both prenatal airborne PAHs and stable aberration frequency in chromosomes 1-6 decreased to half the levels reported previously in the same cohort (mean PAH decreased from 3.6 to 1.8ng/m(3); mean stable aberration frequency from 0.56 to 0.24, SD=0.19). The mean stable aberration frequency was 0.45 (SD=0.15) in chromosomes 11-19. After adjusting for gender, ethnicity, and household smokers, the mean stable aberration frequency increased with increasing PAH exposure: with a doubling of prenatal PAH exposure, the mean stable aberration frequency for the chromosome1-6 group increased by a factor of 1.49 (95% CI: 0.84, 2.66; p=0.17); for chromosomes 11-19 mean stable aberration frequency increased by 2.00 (95% CI: 1.11, 3.62; p=0.02); for chromosome 6 alone, it increased by 3.16 (95% CI: 0.93, 10.77; p=0.06); there was no increase for chromosomes 1-5 (p>0.8). Aberrations in chromosomes 11, 12, 14, 19 and 6 were associated with prenatal exposure to PAHs in air, even at lower levels of PAH in air. The observed chromosome-specific effects of prenatal airborne PAHs raise concern about potential cancer risk.
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