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Dose-dependent relationship between prenatal exposure to fine particulates and exhaled carbon monoxide in
Wiesław A Jędrychowski1, Umberto Maugeri, John Spengler
1Epidemiology and Preventive Medicine, Jagiellonian University Medical College, Kraków, Poland. myjedryc@cyf-kr.edu.pl
Insights
Prenatal exposure to fine particulate matter (PM2.5) is linked to higher exhaled carbon monoxide (eCO) levels in children, suggesting fetal oxidative stress may program heme oxygenase activity.
Area of Science:
- Environmental Health
- Pediatric Pulmonology
- Biomarkers of Exposure
Background:
- Prenatal exposure to fine particulate matter (PM2.5) is a growing concern for child health.
- Exhaled carbon monoxide (eCO) is a potential non-invasive biomarker of oxidative stress.
- Understanding the early-life origins of health outcomes is crucial for preventative strategies.
Purpose of the Study:
- To investigate the association between fetal exposure to PM2.5 and eCO levels in non-asthmatic children.
- To explore potential contributing factors and confounders in this relationship.
Main Methods:
- A cohort of 118 children was studied from birth.
- Prenatal PM2.5 exposure was measured using personal samplers.
- Exhaled carbon monoxide (eCO) was measured at age 7.
- Statistical models accounted for confounders like environmental tobacco smoke (ETS) and respiratory symptoms.
Main Results:
- A significant positive association was found between prenatal PM2.5 exposure and eCO levels (p = 0.042).
- Atopic children exhibited higher eCO levels compared to non-atopic children (p = 0.036).
- Prenatal PM2.5 exposure explained 5.1% of the variability in eCO levels.
Conclusions:
- Elevated eCO in children may stem from fetal oxidative stress due to PM2.5 exposure.
- Heme oxygenase (HO) activity might be programmed during fetal development by fine particulate matter exposure.
- This suggests a potential long-term programming effect of early-life environmental exposures on cellular stress pathways.
Objectives:
The main goal of the study was to assess possible association between fetal exposure to fine particulate matter (PM2.5) and exhaled carbon monoxide (eCO) measured in non-asthmatic children.
Material And Methods:
The subjects include 118 children taking part in an ongoing population-based birth cohort study in Kraków. Personal samplers of PM2.5 were used to measure fine particle mass in the fetal period and carbon monoxide (CO) in exhaled breath from a single exhalation effort at the age of 7. In the statistical analysis of the effect of prenatal PM2.5 exposure on eCO, a set of potential confounders, such as environmental tobacco smoke (ETS), city residence area, sensitization to house dust allergens and the occurrence of respiratory symptoms monitored over the seven-year follow-up was considered.
Results:
The level of eCO did not correlate with the self-reported ETS exposure recorded over the follow-up, however, there was a positive significant relationship with the prenatal PM2.5 exposure (non-parametric trend p = 0.042). The eCO mean level was higher in atopic children (geometric mean = 2.06 ppm, 95% CI: 1.58-2.66 ppm) than in non-atopic ones (geometric mean = 1.57 ppm, 95% CI: 1.47-1.73 ppm) and the difference was statistically significant (p = 0.036). As for the respiratory symptoms, eCO values were associated positively only with the cough severity score recorded in the follow-up (nonparametric trend p = 0.057). In the nested multivariable linear regression model, only the effects of prenatal PM2.5 and cough severity recorded in the follow-up were related to eCO level. The prenatal PM2.5 exposure represented 5.1%, while children's cough represented only 2.6% of the eCO variability.
Conclusion:
Our study suggests that elevated eCO in non-asthmatic children may result from oxidative stress experienced in the fetal period and that heme oxygenase (HO) activity in body tissues may be programmed in the fetal period by the exposure to fine particulate matter.
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