A recent study published in eBioMedicine has delved into the impact of maternal exposure to particulate air pollution on newborn kidney function, specifically by examining cord blood cystatin C levels, an emerging biomarker for kidney health.
The research uncovered that heightened exposure to black carbon (BC) and fine particulate matter (PM2.5) during pregnancy, particularly in the third trimester, correlates with increased cystatin C levels in cord blood. This finding points to potential adverse effects on neonatal kidney function.
Previous studies have postulated that a reduced nephron count at birth may increase the risk of hypertension, with early environmental exposures potentially having long-term health consequences. Proper kidney function is essential for maintaining physiological balance.
However, evaluating renal function in newborns poses challenges. Cystatin C, a protein generated by all nucleated cells and filtered by the kidneys, has emerged as a valuable indicator of glomerular filtration in infants, unaffected by factors such as muscle mass or inflammation.
Ambient air pollution, particularly PM2.5 and BC, has been identified as a major contributor to global health issues, including cardiovascular, respiratory, and renal diseases. PM2.5 has been linked to cardiovascular problems, which are closely intertwined with kidney health.
Maternal exposure to PM2.5 has been associated with increased blood pressure and lower birth weights in newborns, which may impede proper kidney development.
While prior research has demonstrated that air pollution can elevate cystatin C levels and reduce glomerular filtration rates in adults, its effects on neonatal cystatin C levels remain underexplored. This study aimed to bridge this knowledge gap by examining whether gestational exposure to air pollutants such as BC and PM2.5 affects cystatin C levels in neonates.
This study drew on data from 1,484 healthy mother-infant pairs from singleton pregnancies between 2010 and 2020, as part of the ENVIRONAGE (ENVIRonmental influence ON early AGEing) birth cohort in Belgium. Pairs without available cord blood samples or missing relevant data were excluded from the analysis.
To estimate exposure to BC and PM2.5, researchers employed a model that combined satellite land cover data with pollution data from monitoring stations. Daily exposure averages were calculated for the entire pregnancy and by trimester.
Cord blood samples were collected within 10 minutes of birth, stored, and analyzed for cystatin C levels using an immune turbidimetry assay. This technique measures kidney function by quantifying cystatin C levels based on its binding to antibody-coated latex particles.
Statistical analyses, including multiple linear regression, distributed lag models, logistic regression, and sensitivity analyses, were conducted to account for various factors such as maternal age, education level, smoking habits, alcohol consumption during pregnancy, and ethnicity.
The newborns in the study had an average birth weight of 3,417.52 g, with a near-equal distribution of girls (49.6%). The average gestational age was 39.2 weeks. Cystatin C levels in cord blood averaged 2.16 mg/L. Mean exposures to BC and PM2.5 during pregnancy were 1.18 μg/m³ and 12.65 μg/m³, respectively, with exposure levels remaining relatively consistent across trimesters.
Significant associations were identified between exposure to BC throughout pregnancy and elevated cystatin C levels in cord blood, with a 0.5 μg/m³ increase in BC linked to a 0.04 mg/L rise in cystatin C (p<0.01). Similarly, a 5 μg/m³ increase in PM2.5 corresponded to a 0.07 mg/L rise in cystatin C levels (p<0.01).
The first trimester showed an association with BC exposure but not with PM2.5. Sensitivity analyses confirmed that adjusting for additional variables did not significantly alter the observed effects. Importantly, the third trimester (after week 27) was identified as the most critical period for exposure.
Increased exposure to PM2.5 and BC throughout pregnancy, and particularly in the third trimester, was linked to a significant rise in the risk of elevated cystatin C levels, with a 0.5 μg/m³ increase in BC associated with a 37% higher risk and a 5 μg/m³ increase in PM2.5 linked to an 80% higher risk.
The study’s strengths include its large sample size, detailed characterization of participants, prospective follow-up, and the use of a high-resolution spatial air pollution model to estimate fetal exposure. However, the study’s limitation lies in its reliance on cystatin C as the sole marker for kidney function, without incorporating other markers such as creatinine.
In conclusion, this study provides evidence that gestational exposure to PM2.5 and BC, particularly during the third trimester, is significantly associated with elevated cystatin C levels in newborns, suggesting an adverse impact on kidney function from birth.
These findings underscore the importance of monitoring and mitigating early-life exposure to particulate air pollution to safeguard kidney health later in life. The study’s results also highlight the need for further research to inform public health policies aimed at protecting neonatal health.
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