A growing body of literature indicates that childhood exposure to environmental contaminants, such as persistent organic pollutants (POPs), may affect risk of obesity, cardiovascular disease, renal disease, metabolic syndrome, and other chronic diseases.

In a study funded by the National Institute of Environmental Health Sciences, researchers in NYU Langone’s Division of Environmental Pediatrics, led by Leonardo Trasande, MD, MPP, examine the connection between prenatal and postnatal exposure to POPs and childhood heart and kidney dysfunction.

Laboratory studies suggest that POPs such as perfluoroalkyl acids, organochlorine pesticides, polychlorinated biphenyls, and polybrominated diphenyl ethers can disrupt developmental endocrine processes and provoke oxidant stress, a major pathophysiologic mechanism underlying cardiovascular and renal risks. Although some epidemiological studies have investigated exposure to POPs or related contaminants in relation to obesity and cardiovascular effects, older studies may not reflect the effects of current exposures because they preceded phaseout of certain POPs and the emergence of substitutes.

Preliminary analyses suggest associations of perfluoroalkyl acids with sexually dimorphic increases in body mass and reduced glomerular filtration rate. Past studies have also failed to examine interactions and potential joint effects of multiple low-level POP exposures. Few studies have examined these risks in diverse Latinx populations disproportionately affected by obesity, cardiometabolic, and renal risks, including not only Mexican Americans but also other subgroups.

To examine prenatal and childhood POP exposures as cardiometabolic and renal risks, we leverage the resources of Starting Early, an established randomized controlled trial of 533 Latinx mother–infant pairs funded by the U.S. Department of Agriculture (grant number 2011-68001-30207), to examine the association of prenatal and early-life POP exposures with the development of preclinical and intermediate endpoints indicative of early metabolic and cardiorenal risks. We will include at least 400 mother–infant pairs from Starting Early and measure prenatal exposure to POPs using banked newborn blood spots, while adding prospective annual urine and blood collection and clinical visits from age four to seven.

This study provides a unique opportunity to capitalize on existing resources and an engaged study population to evaluate emerging contaminants of concern to young children. We hypothesize that prenatal and childhood exposure to POPs are associated with body mass, elevated blood pressure, increased arterial stiffness, reduced renal function, and increased oxidant stress biomarkers in childhood.

It is possible that alterations detected by such biomarkers can be halted or reversed with modification of risk factors, highlighting the importance of identifying early risk factors and biomarkers of cardiorenal risk in younger populations. With repeated measures of POP exposure during childhood, our extension of the Starting Early study presents a unique opportunity to evaluate cardiovascular and renal effects of early-life exposures.

Public Health Relevance Statement

Exposure to persistent organic pollutants in utero and in early life has the potential to impact long-term heart and kidney health. We propose to examine relationships of prenatal and postnatal exposure to these persistent organic contaminants to a series of biomarkers and preclinical indicators of heart and kidney dysfunction in childhood.