TY - JOUR
T1 - Prenatal blood lead levels and reduced preadolescent glomerular filtration rate
T2 - Modification by body mass index
AU - Saylor, Charlie
AU - Tamayo-Ortiz, Marcela
AU - Pantic, Ivan
AU - Amarasiriwardena, Chitra
AU - McRae, Nia
AU - Estrada-Gutierrez, Guadalupe
AU - Parra-Hernandez, Sandra
AU - Tolentino, Mari Cruz
AU - Baccarelli, Andrea A.
AU - Fadrowski, Jeffrey J.
AU - Gennings, Chris
AU - Satlin, Lisa M.
AU - Wright, Robert O.
AU - Tellez-Rojo, Martha M.
AU - Sanders, Alison P.
N1 - Funding Information:
This work was supported in part by funding from the NIH/NIEHS : K99ES027508 , R00ES027508 , R24ES028522 , P30ES023515 , R01ES013744 , R01ES026033 , and R01ES021357 .
Publisher Copyright:
© 2021 The Author(s)
PY - 2021/9
Y1 - 2021/9
N2 - Background: For the developing kidney, the prenatal period may represent a critical window of vulnerability to environmental insults resulting in permanent nephron loss. Given that the majority of nephron formation is complete in the 3rd trimester, we set out to test whether 1) prenatal lead exposure is associated with decreased preadolescent kidney function and 2) whether preadolescent obesity acts synergistically with early life lead exposure to reduce kidney function. Methods: Our study included 453 mother–child pairs participating in the PROGRESS birth cohort. We assessed prenatal blood lead levels (BLLs) in samples collected in the 2nd and 3rd trimesters and at delivery, as well as tibial and patellar bone lead measures assessed one-month postpartum. Preadolescent estimated glomerular filtration rate (eGFR) was derived from serum levels of creatinine and/or cystatin C measured at age 8–12 years. We applied linear regression to assess the relationship between prenatal bone and BLL with preadolescent eGFR, and adjusted for covariates including age, sex, BMI z-score, indoor tobacco smoke exposure, and socioeconomic status. We also examined sex-specific associations and tested for effect modification by BMI status. Results: We observed null associations between prenatal lead exposure and eGFR. However, in interaction analyses we found that among overweight children, there was an inverse association between BLL (assessed at 2nd and 3rd trimester and at delivery) and preadolescent eGFR. For example, among overweight participants, a one ln-unit increase in 2nd trimester BLL was associated with a 10.5 unit decrease in cystatin C-based eGFR (95% CI: −18.1, −2.8; p = 0.008). Regardless of lead exposure, we also observed null relationships between BMI z-score and eGFR overall, as well as among overweight participants. However, among participants with preadolescent obesity, we observed a significant 5.9-unit decrease in eGFR. We observed no evidence of sex-specific effects. Conclusions: Our findings, if confirmed in other studies, suggest a complex interplay between the combined adverse effects of adiposity and perinatal lead exposure as they relate to adolescent kidney function. Future studies will assess kidney function and adiposity trajectories through adolescence to better understand environmental risk factors for kidney function decline.
AB - Background: For the developing kidney, the prenatal period may represent a critical window of vulnerability to environmental insults resulting in permanent nephron loss. Given that the majority of nephron formation is complete in the 3rd trimester, we set out to test whether 1) prenatal lead exposure is associated with decreased preadolescent kidney function and 2) whether preadolescent obesity acts synergistically with early life lead exposure to reduce kidney function. Methods: Our study included 453 mother–child pairs participating in the PROGRESS birth cohort. We assessed prenatal blood lead levels (BLLs) in samples collected in the 2nd and 3rd trimesters and at delivery, as well as tibial and patellar bone lead measures assessed one-month postpartum. Preadolescent estimated glomerular filtration rate (eGFR) was derived from serum levels of creatinine and/or cystatin C measured at age 8–12 years. We applied linear regression to assess the relationship between prenatal bone and BLL with preadolescent eGFR, and adjusted for covariates including age, sex, BMI z-score, indoor tobacco smoke exposure, and socioeconomic status. We also examined sex-specific associations and tested for effect modification by BMI status. Results: We observed null associations between prenatal lead exposure and eGFR. However, in interaction analyses we found that among overweight children, there was an inverse association between BLL (assessed at 2nd and 3rd trimester and at delivery) and preadolescent eGFR. For example, among overweight participants, a one ln-unit increase in 2nd trimester BLL was associated with a 10.5 unit decrease in cystatin C-based eGFR (95% CI: −18.1, −2.8; p = 0.008). Regardless of lead exposure, we also observed null relationships between BMI z-score and eGFR overall, as well as among overweight participants. However, among participants with preadolescent obesity, we observed a significant 5.9-unit decrease in eGFR. We observed no evidence of sex-specific effects. Conclusions: Our findings, if confirmed in other studies, suggest a complex interplay between the combined adverse effects of adiposity and perinatal lead exposure as they relate to adolescent kidney function. Future studies will assess kidney function and adiposity trajectories through adolescence to better understand environmental risk factors for kidney function decline.
KW - Kidney function
KW - Lead
KW - Obesity
KW - Prenatal
KW - eGFR
UR - http://www.scopus.com/inward/record.url?scp=85107766628&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85107766628&partnerID=8YFLogxK
U2 - 10.1016/j.envint.2021.106414
DO - 10.1016/j.envint.2021.106414
M3 - Article
C2 - 33678412
AN - SCOPUS:85107766628
SN - 0160-4120
VL - 154
JO - Environmental International
JF - Environmental International
M1 - 106414
ER -