The cohort of premature infants evaluated in this study is representative of a susceptible sub-population and the data obtained revealed the presence of several xenobiotics, some even at highly-abundant levels. PFAS are known to readily pass from maternal blood to the developing embryo and are associated with multiple adverse health outcomes during pregnancy, including low birth weight caused by impaired placental function . Potential sources of exposure to plasticizers include contact with medical equipment such as ventilators, feeding tubes and infusion pumps in the neonatal ICU. High paraben levels may derive from the injection of pharmaceuticals that include them as excipients or preservatives . The detection of cotinine in 20 individuals from the cohort points towards the possibility of systemic passive exposure to smoke. At first glance, this was a particularly unexpected outcome. Although it was not possible to accurately quantitate cotinine using matrix-matched calibration (high contamination of the commercially-available pooled human serum used for calibration purposes); by applying solvent calibration, levels <0.5 ng mL -1 were estimated for all samples. This is consistent with previous findings of mean cotinine levels in non-smokers as a result of everyday exposure to passive smoking . The contamination of donated, pooled breast milk that is routinely used as a supplement in the clinic may be a source of this ubiquitous contamination, although active smokers are excluded as milk donors. This hypothesis is reinforced by the identification of both nicotine metabolites cotinine and trans-3-hydroxy cotinine in the breast milk that was applied for matrix-matched calibration (Supplementary Figure ). However, this breast milk pool was provided by a different clinic and was not the pool that had been fed to the neonate cohort (see Online Methods). Although synthetic xenobiotics comprise the majority of the quantitated chemicals, the simultaneous detection of HMF and HMFA in one individual demonstrated the successful quantitation of a food carcinogen and the main human metabolite thereof. We surmised that the pasteurization process of the donor milk during preparation for the premature babies may have led to the pyrolytic formation of HMF; and the infant was subsequently exposed during ingestion. It is highly likely that contaminated milk may have also resulted in the ingestion of a limited number of phyto-and mycoestrogens at low concentrations.