The study drew on 289 children enrolled in the PROGRESS cohort in Mexico, a long-running birth cohort designed to examine how environmental exposures shape child health. Rather than relying on blood or urine samples, which capture only recent exposure, the researchers turned to deciduous teeth, the baby teeth that children naturally shed. Teeth grow in layers much like tree rings, and the dentine that forms during specific developmental periods locks in a chemical record of what circulated in the child’s bloodstream at the time. By segmenting dentine along growth lines, the team was able to retrospectively quantify arsenic exposure for every week from sixteen weeks before birth through fourteen weeks after birth, an unprecedented temporal resolution for an immunotoxicology study.

When the children returned for a follow-up visit around age four to five, the investigators measured serum levels of immunoglobulin G antibodies directed against six vaccine antigens: measles, mumps, and rubella from the MMR vaccine, and diphtheria, tetanus, and pertussis from the DTP series. These antibodies are the immune system’s memory of vaccination, the molecular shield that prevents re-infection, and their concentrations in blood are a standard benchmark of how well a vaccine has taken hold. The measurements were performed using a multiplexed Luminex bead-based immunoassay, a technique that allows all six antibody targets to be quantified simultaneously from a small serum sample.

The statistical challenge was considerable. Because arsenic exposure was estimated for thirty consecutive weeks, the researchers needed a method that could detect when in that timeline exposure mattered, not just whether it mattered overall. They employed Distributed Lag Non-linear Models, or DLNMs, a framework originally developed in environmental epidemiology for studying delayed and time-varying effects of air pollution and temperature. The models related log2-transformed dentine arsenic concentrations to log2-transformed antibody levels across every week of the perinatal period, while adjusting for the child’s age, maternal education, parity, and child sex. The log2 transformation means the reported effects can be read as the change in antibody level associated with a doubling of arsenic exposure during a given week.

The results converged on a single, well-defined period. A doubling of arsenic exposure in the window spanning one week before birth to six weeks after birth was associated with significantly lower anti-measles antibody levels, with an estimated effect of minus 5.62 on the log2 scale and a 95 percent confidence interval running from minus 8.39 to minus 0.83. The same perinatal window showed a significant association for anti-rubella antibodies, with an effect estimate of minus 3.85 and a confidence interval from minus 6.99 to minus 0.63. In practical terms, children with higher arsenic exposure in the weeks surrounding delivery carried measurably weaker antibody defenses against measles and rubella years later, even though their vaccinations occurred long after the exposure itself.

Just as telling was what the analysis did not find. Arsenic exposure during the perinatal window showed no significant association with antibody levels against mumps, diphtheria, tetanus, or pertussis. Nor did earlier or later periods of prenatal and early postnatal exposure produce significant signals for any antigen. This selectivity is biologically intriguing. It suggests that the immune pathways supporting long-term antibody maintenance against measles and rubella may be more sensitive to arsenic’s interference than those supporting the other four antigens, or that different vaccine antigens rely on differently timed developmental programs of B-cell and plasma-cell maturation that vary in their vulnerability to toxic insult.

The timing of the susceptible window makes biological sense. The weeks surrounding birth are a period of profound immunological transition. The fetus must shift from the sterile, maternally protected environment of the womb to an microbe-rich world, and neonatal immune cells are actively learning to distinguish threat from tolerance. Maternal antibodies transferred across the placenta are waning while the infant’s own antibody production is just beginning. Arsenic is known to disrupt immune signaling, generate oxidative stress, and interfere with methylation processes that regulate gene expression, and a toxic exposure during this delicate choreography could plausibly leave a lasting imprint on how well vaccine memory is established and maintained.

The researchers also probed whether the effects differed between boys and girls, or between children who were breastfed at one month postpartum and those who were not, since both factors can shape immune development and arsenic dynamics. They found no heterogeneity by either sex or breastfeeding status, indicating that the association between perinatal arsenic and reduced measles and rubella antibodies appears to operate similarly across these subgroups. That consistency strengthens the case that the finding reflects a general biological vulnerability rather than an effect confined to a particular subset of children.

The methodological innovation deserves particular attention. Traditional exposure assessment in environmental health has long been hampered by the difficulty of reconstructing what a person was exposed to years or decades earlier. Baby teeth offer a solution that is both retrospective and precise, and their use here demonstrates how naturally shed biomaterials can transform the study of developmental toxicology. Combined with the DLNM framework, which treats exposure timing as a variable to be mapped rather than averaged, the approach allowed the team to draw a temporal map of vulnerability with weekly resolution, something conventional single-biomarker studies simply cannot achieve.

The public health implications are significant. Measles remains one of the most contagious human pathogens, and even modest reductions in population-level antibody levels can erode herd immunity and fuel outbreaks, a concern made vivid by recent resurgences of measles in countries where the disease was once controlled. Arsenic contamination of groundwater affects an estimated hundreds of millions of people worldwide, and in regions such as Mexico, where the PROGRESS cohort is based, exposure often begins before birth. If the findings are confirmed in other cohorts, they would add vaccine-preventable disease susceptibility to the long list of harms attributable to early-life arsenic exposure, and they would sharpen the argument for reducing arsenic exposure among pregnant women and newborns, whether through water filtration, dietary interventions, or regulatory limits on contaminated sources. The study, funded by the National Institutes of Health and led by researchers at the Icahn School of Medicine at Mount Sinai together with collaborators at Mexico’s National Institute of Public Health and other institutions, was published open access, with the authors reporting no competing interests.

Subject of Research: Perinatal arsenic exposure and vaccine-specific antibody levels in children

Article Title: Susceptible perinatal windows to arsenic exposure and serum antibody levels in children

Article References: Scotti, A., India-Aldana, S., Martinez, M., Arora, M., McRae, N., Lamadrid-Figueroa, H., Quataert, S. A., Estrada-Gutierrez, G., Torres-Olascoaga, L., Téllez-Rojo, M. M., Wright, R. O., Jusko, T. A., & Colicino, E. (2026). Susceptible perinatal windows to arsenic exposure and serum antibody levels in children. Environmental Health. https://doi.org/10.1186/s12940-026-01331-6

Image Credits: AI Generated

DOI: 10.1186/s12940-026-01331-6

Keywords: arsenic exposure, perinatal window, vaccine antibodies, measles, rubella, immunotoxicology, baby teeth, dentine, PROGRESS cohort, DLNM, humoral immunity, environmental health