RESUMEN
As an alternative to bisphenol A (BPA), bisphenol S (BPS) has been used as an ink developer in thermal paper products including price labels on food packaging which have been suggested as the sources of BPS found at high levels in packaged fish samples. BPS in the printed price labels glued onto the outside of plastic film could migrate indirectly from the printed surface through the paper, adhesive and film into the food. In order to investigate if price labels could also be the sources of BPS detected in the meat samples in our previous studies, meat and other food samples packaged under different conditions were collected, and BPS in these samples together with the price labels on the corresponding packaging were extracted with solvent followed by solid phase extraction and stable isotope dilution LC-MS/MS analysis. BPS was detected at very high levels (161.7-222.4 µg/cm2) in all the five sticker type of price labels, indicating BPS being the dominant if not the sole ink developer. BPS was also detected in all the 26 continuous roll type of price labels but at very low levels (0.017-18 ng/cm2), indicating that the dominant ink developer is likely one of the other alternatives, rather than BPS. Despite BPS being detected in all price labels on packaging of fish, meat, and cheese samples, BPS was not detected or detected in only a few fish, meat, and cheese samples at levels considerably lower than the current EU specific migration limit (SML) of 50 ng/g food for BPS authorised under Regulation (EU) 10/2011.
RESUMEN
BACKGROUND: Parathyroid hormone (PTH) is an indirect functional indicator of vitamin D status. Risk of vitamin D deficiency, assessed using circulating 25-hydroxyvitamin D (25(OH)D), is defined as <30 nmol/L by the National Academy of Medicine and alternatively <25 nmol/L in the global consensus recommendation on prevention and management of nutritional rickets. OBJECTIVE: To test PTH concentrations and the odds for elevated values according to vitamin D deficiency cut-points (<30 nmol/L, or <25 nmol/L) in newborn infants. METHODS: Healthy term-born infants (n = 858) were recruited from Montreal, Canada (2016-2019). Obstetric data were obtained from medical records, and demographic factors surveyed. Immunoassays were used to measure newborn (24-36 h) serum PTH and 25(OH)D; 25(OH)D was standardized to National Institute of Standards and Technology (NIST) standard reference materials. Serum PTH was log-transformed before comparing serum 25(OH)D groups (<30 vs. ≥30; or <25 vs. ≥25 nmol/L) using ANCOVA adjusted for infant sex, type of delivery, parity, race, and family income. The odds of elevated PTH (>71.48 pg/mL) were tested using logistic regression, adjusted for the same covariates. RESULTS: Infants (50.2 % female) were 39.6 ± 1.0 weeks gestational age (mean ± SD), and 3.41 ± 0.38 kg. Median serum 25(OH)D was 45.4 (IQR 23.2) nmol/L; 20.5 % had serum 25(OH)D < 30 nmol/L, and 12.4 % <25 nmol/L. Median serum PTH was 30.72 (IQR 33.90) pg/mL, elevated in 12.7 % overall, and higher in infants born with serum 25(OH)D < 25 vs. ≥25 nmol/L (35.96 (IQR 39.20) vs. 30.36 (IQR 32.93) pg/mL, p = 0.0158). The odds of elevated PTH were higher when serum 25(OH)D was <25 nmol/L (ORadj 2.13, 95 % CI: 1.23, 3.69). PTH concentration and the odds of being elevated did not differ according to the 30 nmol/L cut-point. CONCLUSIONS: Based on this study, the definition of vitamin D deficiency relative to bone health as set by the National Academy of Medicine (<30 nmol/L) exceeds the threshold at which PTH is elevated in newborn infants.