BACKGROUND:Some epidemiological studies suggest that phthalates adversely affect children's neurodevelopment, but results are inconsistent and often only consider individual chemicals. OBJECTIVES:We examined associations between gestational phthalate metabolites and intelligence at ages 3-4 and investigated effect modification by child sex. METHODS:We analyzed data from 511 mother-child pairs enrolled in the Maternal-Infant Research on Environmental Chemicals study. We measured specific gravity-standardized urinary concentrations of 20 phthalate metabolites (from nine parent compounds) in trimesters 1 and 2 and computed the average. We used linear regression models (log2-transformed), adjusting for covariates, to examine single-chemical associations with Full-Scale (FSIQ), Performance (PIQ), and Verbal IQ (VIQ) measured by the Weschler Preschool and Primary Scale of Intelligence-III. We estimated mixture effects using weighted quantile sum (WQS) regression. RESULTS:Detection frequencies of the metabolites ranged from 42 to 99%. In single-chemical analyses, the sum of di-isodecyl phthalate metabolites (ΣDiDPm) was associated with decreased FSIQ (-0.5, 95%CI: -2.1, -0.0) and PIQ (-0.6, 95%CI: -1.2, -0.0). Monomethyl phthalate (MMP) was associated with increased FSIQ (1.7, 95%CI: 0.4, 3.1), PIQ (1.7, 95%CI: 0.2, 3.1) and VIQ; (1.6, 95%CI: 0.3, 2.8). Monobenzyl phthalate (MBzP) was positively associated with PIQ (0.9, 95%CI: 0.0, 1.9). Associations between ΣDiDPm and VIQ and MMP and PIQ differed by child sex (negative for boys and positive for girls, respectively). WQS analyses were not statistically significant. CONCLUSIONS:Findings from this pan-Canadian cohort provide some evidence that gestational ΣDiDPm is adversely associated with child cognition, with sex-specific vulnerabilities. The positive associations with MMP and MBzP warrant further research.

OBJECTIVE:Glyphosate is the most widely used pesticide worldwide. Few epidemiologic studies have examined the potential for neurotoxicity by glyphosate or its degradate, Aminomethylphosphonic Acid (AMPA). We examined associations of maternal urinary glyphosate and AMPA concentrations with child cognitive, social, and behavioural functioning in participants enrolled in the Maternal-Infant Research on Environmental Chemicals (MIREC) study. METHODS:Maternal urinary glyphosate and AMPA concentrations were measured in first trimester spot urine samples. We assessed children's cognition (IQ) at 3-4 years of age (n = 572) using the Wechsler Preschool and Primary Scale of Intelligence-III. Social (n = 566) and behavioural (n = 840) functioning were assessed using parent-report versions of the Social Responsiveness Scale-2 and Behavioral Assessment System for Children-2. We quantified associations between maternal urinary glyphosate and AMPA concentrations and child neurodevelopmental outcomes using multivariable linear regression models and assessed effect modification by child sex, maternal folic acid, and plasma folate. RESULTS:Median (IQR) urinary glyphosate and AMPA concentrations were 0.31 (0.33) μg/L and 0.25 (0.25) μg/L. Maternal urinary glyphosate and AMPA concentrations were not significantly associated with children's cognitive, social or behavioural functioning, and there was no evidence of effect modification. We found a non-significant inverse trend between maternal urinary AMPA concentrations and Performance IQ (B = -0.85; 95 %CI: -1.71,0.01). CONCLUSION:In this primarily urban cohort of Canadian mother-child pairs, prenatal glyphosate and AMPA exposure were not significantly associated with child neurodevelopment. Further evaluation of glyphosate as a potential developmental neurotoxicant in a study with multiple urine samples per participant and at higher exposure levels is warranted.

Studies on prenatal exposure to per- and polyfluoroalkyl substances (PFAS) and cardiometabolic health in childhood have produced inconsistent results. In this study, we evaluated associations between prenatal PFAS exposures, individually and as a mixture, and cardiometabolic outcomes including insulin resistance, beta cell function, blood lipids, blood pressure and central adiposity during middle childhood (7-9 years of age) in a Canadian maternal-child cohort (n = 281). We also explored effect measure modification based on child sex and physical activity. We quantified maternal second trimester plasma concentrations of six PFAS and measured 11 offspring cardiometabolic outcomes at a 7-9-year follow-up. In single-exposure models, ten-fold higher prenatal PFDA (β: -0.82, 95% CI: -1.36, -0.28), PFNA (β: -0.8, 95% CI: -1.41, -0.19), and PFOA (β: -0.69, 95% CI: -1.18, -0.19) concentrations were associated with lower diastolic blood pressure z-scores. This association did not persist when considering PFAS exposures as a mixture using quantile g-computation. Associations between PFAS exposures, individually or as a mixture, and other cardiometabolic outcomes were null. We observed no effect measure modification by child sex or physical activity (p-values for interaction ≥0.2). Our results contradict existing studies that suggest prenatal PFAS exposures are associated with adverse childhood cardiometabolic outcomes. Future studies should consider alternative markers of cardiometabolic health, trajectories in cardiometabolic health throughout childhood, and further explore potentially protective health behaviors.

Background:Prenatal exposure to environmental chemicals may be associated with autism or autistic-like behaviors. Previous studies suggest that these associations are stronger when folic acid (FA) supplementation is lower. Methods:We used data from the Maternal-Infant Research on Environmental Chemicals study, a Canadian pregnancy and birth cohort (2008-2011). We considered five separate chemical mixtures (measured during the first trimester of pregnancy): metals, organochlorine pesticides, per- and polyfluoroalkyl substances (PFAS), polychlorinated biphenyls (PCBs), and persistent organic pollutants (POPs; including organochlorine pesticides, PFAS, PCBs, and one polybrominated diphenyl ether congener). Autistic-like behaviors were documented in 601 3-4-year-old children with the social responsiveness scale-2 (SRS-2), where higher T-scores denote more behaviors. We used quantile g-computation to estimate the mixture-SRS-2 associations and assessed whether gestational FA supplementation and plasma total folate concentrations modified these associations. Results:The PFAS mixture was associated with decreased SRS-2 T-scores (Ψ = -0.5; 95% confidence interval [CI] = -1.1, 0.1). The metal-SRS-2 associations were stronger in the positive direction among participants with high (>1,000 μg/d) FA supplementation (Ψ = 2.4; 95% CI = 0.8, 3.9) versus those with adequate (400-1,000 μg/d) supplementation (Ψ = -0.2; 95% CI = -1.1, 0.7) (p-interaction = 0.003). Plasma total folate concentrations similarly modified these associations (p-interaction = 0.01). The associations between the PFAS, PCB, and POP mixtures and SRS-2 T-scores were stronger in the positive direction among participants with low (<400 μg/d) versus adequate FA supplementation. This was not observed when assessing modification by plasma total folate concentrations. Conclusion:Our results suggest that the metal mixture is more strongly associated with autistic-like behaviors among participants with higher folate exposure, and the PFAS, PCB, and POP mixtures are more strongly associated with autistic-like behaviors among participants with low FA supplementation.

The solvents N-methyl-2-pyrrolidone (NMP) and N-ethyl-2-pyrrolidone (NEP) are established developmental toxicants; however, epidemiological data are lacking. We quantified associations between urinary NEP and NMP metabolites concentrations and pregnancy outcomes in participants enrolled in the pan-Canadian Maternal-Infant Research on Environmental Chemicals study (n = 1865) (2008-2011). Using discrete time survival analysis and logistic regression, we calculated the odds of preterm birth (PTB) and fetal loss. We used multivariable linear regression to quantify associations between metabolites and birth weight z-scores. Participants with quantifiable concentrations of the NEP metabolite 5-hydroxy-N-ethyl-2-pyrrolidone (5-HNEP) had a 41% increased odds of PTB (95% CI: 0.92-2.17). An interquartile range increase in concentrations of the NMP metabolite 5-hydroxy-N-methyl-2-pyrrolidone (5-HNMP) was associated with a reduced odds of fetal loss (OR = 0.51 95% CI: 0.30,0.89). All other effect estimates were centered around the null value. We report widespread, low-level exposure to NMP metabolites yet no evidence of adverse effects on fetal health. Our analysis of fetal loss was most likely subject to selection bias resulting from conditioning on pregnancies with available first trimester urine samples Our finding that 5-HNEP exposure may increase risk of preterm birth provides impetus for further biomonitoring and etiological research in a pregnant population with contemporary NEP exposure.

BACKGROUND:Exposure to toxic elements and deficiencies/excessive exposure to essential elements is associated with adverse health effects. Robust biomonitoring data exist for select elements in the general population of Canada, but data are limited for several essential/trace elements, especially among females approaching menopause, a critical and understudied life stage. OBJECTIVE:To describe whole blood concentrations of toxic, essential, and trace elements in females enrolled in a 2018-2021 follow-up of the Canadian Maternal-Infant Research on Environmental Chemicals cohort, and examine differences in concentrations by sociodemographic and obstetrical history characteristics. METHODS:We analyzed whole blood samples (n = 288) for concentrations of 21 elements. For 14 elements with >50% detection, we calculated Spearman correlations and compared geometric means across strata of participant characteristics. RESULTS:Element concentrations were similar or lower than reported for similarly aged females in Canada. Participants seemed to have adequate concentrations of essential elements except for zinc, where most were below the proposed zinc adequacy biomonitoring equivalent (6017 μg/L whole blood). The strongest correlations (ρ = 0.41-0.63) were observed between toxic elements which may share exposure sources (mercury/arsenic), and essential elements associated with blood cell production/function (iron/cobalt/copper/zinc/manganese/selenium). Participants' geometric mean element concentrations were generally 1.1-2.0 times higher among peri-/post-menopausal participants (lead), those with unknown menopausal status (iron), older participants (cadmium), younger participants (iron, beryllium), smokers (lead, cadmium), non-smokers (selenium), lower BMI (lead, mercury, arsenic, cesium), higher BMI (manganese, copper), higher household income (nickel), and higher education (mercury, arsenic, cesium). CONCLUSIONS:We provide important biomonitoring data for elements among adult females approaching the menopausal transition.

BACKGROUND:Legacy per- and polyfluoroalkyl substances (PFAS) can promote dyslipidemia; however, evidence is lacking for alternative and precursor PFAS. We investigated associations between serum concentrations of 31 PFAS and concurrently measured lipids and liver function biomarkers. METHODS:PFAS, lipids, and liver function biomarkers were analyzed in serum samples provided by 282 adult females participating in a 2018-2021 follow-up study of a Canadian pregnancy cohort. We examined percent differences in outcomes continuously for 17 PFAS with >50% detection and as detected vs. not detected for 14 PFAS with 10-50% detection. We also examined associations with the sum of 7 PFAS recommended by the National Academies of Sciences, Engineering, and Medicine guidance report on PFAS testing and 17 PFAS. We used weighted quantile sum (WQS) and quantile g-computation models to estimate joint associations. RESULTS:Each two-fold increase in concentrations of PFHxS, PFOS, PFNA, PFDA, PFHpS, and Σ7PFAS were associated with up to 7% higher total and LDL cholesterol and the TC:HDL ratio. Individuals with detectable concentrations of N-EtFOSA, N-MeFOSA, PFBS, and 9Cl-PF3ONS had up to 17% higher total and LDL cholesterol and TC:HDL. Each one-quartile increase in the mixture of 7 PFAS was associated with up to 10% higher total and LDL cholesterol. Adding additional PFAS to the mixture (17 PFAS) made estimates less precise in WQS models and attenuated associations to the null in quantile g-computation models. CONCLUSION:Alternative and precursor PFAS, including replacements for legacy PFAS, are associated with higher cholesterol levels; prospective studies are required to confirm these findings.

Context During pregnancy, women who experience certain pregnancy complications show elevations in biomarkers of inflammation and insulin resistance; however, few studies have examined these cardiometabolic biomarkers in the decade following pregnancy.Objective To examine the association between pregnancy complications and cardiometabolic biomarkers 9 years postpartum including blood pressure, blood lipids, body fat percentage, insulin resistance [glucose, insulin, proinsulin, C-peptide, Homeostasis Model Assessment of Insulin Resistance (HOMA-IR), glycated hemoglobin (HbA1c), leptin, adiponectin], and inflammation (high-sensitivity-C-reactive protein).Methods Using data from the Maternal-Infant Research on Environmental Chemicals cohort study (2008-2021), we determined 3 groups of pregnancy complications: (1) hypertensive disorders of pregnancy (HDP) (n = 35); (2) any pregnancy complication in the index pregnancy, defined as preterm birth, HDP, impaired glucose tolerance or gestational diabetes mellitus (n = 55); and (3) self-reported recurrence of 1 of these pregnancy complications (n = 19). Our comparison group included 186 women with uncomplicated pregnancies.Results In our adjusted linear regression results, all pregnancy complication groups showed significantly higher systolic and diastolic blood pressure 9 years later. HOMA-IR was 23% [95% confidence interval (CI): -4.4%, 57%], 26% (95% CI: 2.0%, 55%), and 51% (95% CI: 12%, 104%) higher at follow-up in participants who had experienced a prior HDP, an index pregnancy complication, or a recurrent pregnancy complication, respectively. Elevations were also seen with HbA1c, insulin, C-peptide, and leptin, especially among those with recurrent complications.Conclusion This study contributes to the body of evidence that women with a history of certain pregnancy complications merit special attention in the prevention of cardiovascular disease. We recommend further exploration into these associations in larger cohorts.

BACKGROUND:Ochratoxin A (OTA) is a mycotoxin produced by multiple fungal species and is found in a variety of foods. Ingestion of OTA-contaminated foods by lactating mothers can lead to OTA exposure in infants. METHODS:To help assess infants' exposure to OTA, milk samples from the Maternal-Infant Research on Environmental Chemicals (MIREC) Human Milk Study were analyzed. Human milk samples were collected (n = 494) and analyzed for OTA levels by HPLC. RESULTS AND DISCUSSION:The mean OTA concentration was 7.32 ± 9.25 ng/L, with 390 (79%) test samples testing positive for OTA and a range of 4.5-192 ng/L. Based on the food consumption questionnaires distributed among participants, higher OTA levels were observed with higher consumption of cottage cheese, hot cereal, and whole-grain bread and significant differences were found in OTA levels at different sites. The mean OTA level in the analyzed milk test samples was well below the amount found in infant formulas sold in Canada, which was determined by Health Canada to be safe. CONCLUSIONS:The concentrations of OTA found in human milk in this study are well below the amount deemed safe in infant formula by Health Canada and, therefore, unlikely to be of concern to infant health.

Background: Folic acid (FA) supplementation may attenuate the associations between gestational exposure to certain chemicals and autism or autistic-like behaviors, but to our knowledge, this has not been assessed for lead. Objectives: We examined whether the relationship between gestational blood-lead levels (BLLs) and autistic-like behaviors was modified by gestational plasma total folate concentrations, FA supplementation, and maternal methylenetetrahydrofolate reductase (MTHFR) 677C>T genotype. Methods: We used data from the Maternal-Infant Research on Environmental Chemicals study (2008-2011), a Canadian pregnancy and birth cohort study. Childhood autistic-like behaviors were documented in 601 children 3-4 y of age with the Social Responsiveness Scale-2 (SRS-2), where higher scores denote more autistic-like behaviors. We measured BLLs and plasma total folate concentrations during the first and third trimesters of pregnancy. We also estimated gestational FA supplementation via surveys and genotyped the maternal MTHFR 677C>T single nucleotide polymorphism (SNP). We estimated the confounder-adjusted associations between log2-transformed BLLs and SRS-2 scores by two indicators of folate exposure and maternal MTHFR 677C>T genotype using linear regression. Results: Third-trimester BLLs were associated with increased SRS-2 scores [beta(adj)=3.3; 95% confidence interval (CI): 1.1, 5.5] among participants with low (<10th percentile), third-trimester, plasma total folate concentrations, but BLL-SRS-2 associations were null (beta(adj)=-0.3; 95% CI: -1.2, 0.5) among those in the middle category (>= 10th and <80th percentiles) (p-interaction <0.001). FA supplementation also attenuated these associations. Both folate indicators modified first-trimester BLL-SRS-2 associations, but to a lesser extent. Third-trimester BLL-SRS-2 associations were slightly stronger among participants who were homozygous for the T (minor) allele of the MTHFR 677C>T SNP (beta(adj)=0.9; 95% CI: -1.2, 3.1) than those without the T allele (beta(adj)=-0.3; 95% CI: -1.3, 0.7), but the difference was not statistically significant (p-interaction=0.28). Discussion: Folate may modify the associations between gestational lead exposure and childhood autistic-like behaviors, suggesting that it mitigates the neurotoxic effects of prenatal lead exposure.

Polybrominated diphenyl ethers (PBDEs) and hexabromocyclododecane (HBCD) were measured in 298 human milk samples collected from across Canada between 2008 and 2011 as part of the Maternal-Infant Research on Environmental Chemicals study. PBDEs were detected in 100% of the samples analyzed and concentrations ranged from 0.071 to 267 ng·g-1 lipid (median 15.6 ng·g-1 lipid). The dominant contributors to ΣPBDEs (Σ15, 17, 28, 37, 47, 66, 71, 75, 77, 85, 99, 100, 119, 138, 153, 154, 160, 183, 190, 209) were PBDE 47 > PBDE 153 > PBDE 99 > PBDE 100 > PBDE 28 > PBDE 209. Previously, PBDE 209 was considered to be a minor contributor to ΣPBDE concentrations in Canadian human milk and, therefore, not reported by our lab. This study showed that when present, PBDE 209 can be an important contributor to ΣPBDEs (range: below detection - 85.3 ng·g-1 lipid; median - 0.083 ng·g-1 lipid). ΣPBDE concentrations declined slightly in Canadian human milk between the early and late 2000s. HBCD (Σ of α-, β-, and γ-) was observed in 94.0% of the samples measured and concentrations were dominated by α-HBCD (93.3%), with β- (9.7%) and γ- (28.5%) less frequently detected. The maximum ΣHBCD concentration observed was 7.66 ng·g-1 lipid (median value 0.303 ng·g-1 lipid). These data suggest that HBCD concentrations similarly decreased in Canadian human milk between the early 2000s and sampling for the present study. Maternal age did not impact the concentrations of these flame retardants in milk. Additionally, other maternal characteristics [e.g., the number of children a woman has had, pre-pregnancy body mass index (BMI), and education level] did not impact concentrations of these brominated flame retardant concentrations.

Background Gestational exposure to toxic environmental chemicals and maternal social hardships are individually associated with impaired fetal growth, but it is unclear whether the effects of environmental chemical exposure on infant birth weight are modified by maternal hardships. Methods We used data from the Maternal-Infant Research on Environmental Chemicals (MIREC) Study, a pan-Canadian cohort of 1982 pregnant females enrolled between 2008 and 2011. We quantified eleven environmental chemical concentrations from two chemical classes – six organochlorine compounds (OCs) and five metals – that were detected in ≥ 70% of blood samples collected during the first trimester. Using birth weight adjusted for gestational age (GA) as our outcome, we assessed nine maternal hardships by questionnaire. Each maternal hardship variable was dichotomized to indicate whether the females experienced the hardship. In our analysis, we used elastic net to select the environmental chemicals, maternal hardships, and 2-way interactions between maternal hardships and environmental chemicals that were most predictive of birth weight. Next, we obtained effect estimates using multiple linear regression, and plotted the relationships by hardship status for visual interpretation. Results Elastic net selected trans-nonachlor, lead, low educational status, minority status, and low supplemental folic acid intake. All were inversely associated with birth weight. Elastic net also selected interaction terms. Among those with increasing environmental chemical exposures and reported hardships, we observed stronger negative associations and a few positive associations. For example, every two-fold increase in lead concentrations was more strongly associated with reduced infant birth weight among participants with low educational status (β = -100 grams (g); 95% confidence interval (CI): -215, 16), than those with higher educational status (β = -34 g; 95% CI: -63, -3). In contrast, every two-fold increase in mercury concentrations was associated with slightly higher birth weight among participants with low educational status (β = 23 g; 95% CI: -25, 71) compared to those with higher educational status (β = -9 g; 95% CI: -24, 6). Conclusions Our findings suggest that maternal hardships can modify the associations of gestational exposure to some OCs and metals with infant birth weight.

Objective: To study the association between maternal exposure to arsenic, cadmium, lead, manganese and mercury, time-to-pregnancy (TTP) and infertility.Design: Pregnancy-based retrospective TTP cohort study.Setting: Hospitals and clinics from ten cities across Canada.Population: A total of 1784 pregnant women.Methods: Concentrations of arsenic, cadmium, lead, manganese and mercury were measured in maternal whole blood during the first trimester of pregnancy as a proxy of preconception exposure. Discrete-time Cox proportional hazards models generated fecundability odds ratios (FOR) for the association between metals and TTP. Logistic regression generated odds ratios (OR) for the association between metals and infertility. Models were adjusted for maternal age, pre-pregnancy body mass index, education, income, recruitment site and plasma lipids.Main Outcome MeasuresTTP was self-reported as the number of months of unprotected intercourse to become pregnant. Infertility was defined as TTP longer than 12 months.Results: A total of 1784 women were eligible for the analysis. Mean +/- SD maternal age and gestational age at interview were 32.2 +/- 5.0 years, and 11.6 +/- 1.6 weeks, respectively. Exposure to arsenic, cadmium, manganese or mercury was not associated with TTP or infertility. Increments of one standard deviation of lead concentrations resulted in a shorter TTP (adjusted FOR 1.09, 95% CI 1.02-1.16); however, the association was not linear when exposure was modelled in tertiles.Conclusion: Blood concentrations of metals at typical levels of exposure among Canadian pregnant women were not associated with TTP or infertility. Further studies are needed to assess the role of lead, if any, on TTP.

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Exposure to per- and polyfluoroalkyl substances (PFAS) is ubiquitous and may be associated with neurodevelopmental toxicity. However, epidemiological studies report mixed results on the risks of gestational PFAS exposure for children's neurobehavioral impairment. We aimed to examine the associations between prenatal PFAS exposure and children's neurobehavioral and social problems. We measured plasma concentrations of perfluorooctanoate (PFOA), perfluorooctane sulfonate (PFOS), and perfluorohexane sulphonate (PFHxS) in first-trimester blood from 757 women from the Canadian Maternal-Infant Research on Environmental Chemicals (MIREC) study. Children were assessed at 3-4 years with the Behavior Assessment System for Children-2 (BASC-2) and the Social Responsiveness Scale-2 (SRS-2) (n = 756 and 496, respectively). We used multivariable linear regression to examine associations between individual and summed log2-transformed PFAS and scores on these assessments. Effect modification by sex was evaluated through interaction terms and stratified analyses. In the sample combining both sexes, a doubling of maternal PFOA was significantly associated with lower T-scores on the following SRS-2 scales: Social Motivation, DSM-Social Communication, and SRS Total score (B ranging from -1.08 to -0.78), suggesting lesser impairments with higher exposure. In sex-stratified analysis, PFOA was related to significantly lower T-scores in boys for these BASC-2 scales: Behavioral Symptoms Index, Externalizing Problems, Aggression, and Hyperactivity (B ranging from -1.32 to -1.03). In girls, however, PFAS were associated with more problem behaviors, but most associations were small and the CIs included the null, with the exception of PFOA being significantly associated with higher T-scores for the BASC-2Anxiety scale (B = 1.84, 95% CI: 0.36, 3.32). In conclusion, we did not observe strong associations between prenatal exposure to the PFAS evaluated and children's neurobehavioral and social development in this population with low exposure levels. The results show mixed findings, depending on children's sex, neurodevelopmental outcome, and specific PFAS.

Background: Human milk (HM) composition data are widely used in clinical, regulatory, and public health initiatives. The existing HM profiles in United States and Canadian nutrient databanks are outdated and now considered inappropriate to estimate current nutrient intakes. Recent reviews have underscored the limited North American data available to generate a new profile. Objectives: To describe concentrations and sources of variability of nutrients in HM from a large cohort collected in Canada. Methods: The Maternal-Infant Research on Environmental Chemicals (MIREC) study recruited participants in the fi rst trimester of pregnancy from 10 Canadian cities between 2008 and 2011. HM samples (n 1 / 4 559-835, depending on nutrient) were collected 3-10 wk postpartum and analyzed for minerals (calcium, magnesium, phosphorus, potassium, sodium, manganese, molybdenum, zinc, copper, iodine, selenium), vitamin D [vitamin D-3, 25hydroxyvitamin D-3], folate vitamers (folic acid, 5-methyltetrahydrofolate, total folates), and fatty acids (panel). We examined associations between participant characteristics and log-transformed nutrient concentrations using linear regression. Results: Concentrations of HM components in MIREC samples were within the range observed in literature except for manganese, which was > 100-fold lower than the value in the existing Canadian nutrient databank profile [2.43 (standard deviation 2.84) compared with 260 ng/g]. In multivariable models, concentrations of folate vitamers, vitamin D, and fatty acids demonstrated greater variability with maternal and sample characteristics than minerals. Factors such as relevant supplement use, body mass index, and for vitamin D, skin color and season, had a larger impact on nutrient concentrations than characteristics typically standardized in HM research, such as maternal or infant health, and method of collection. Conclusions: HM mineral concentrations from this study meet the methodological inclusion criteria for updating nutrient databank values and dietary reference intakes. Consideration of factors such as diet, skin color, and BMI will be important for selecting studies for developing representative reference values based on HM.

Background Per- and polyfluoroalkyl substances (PFAS) are ubiquitous chemicals routinely detected in personal care products (PCPs). However, few studies have evaluated the impact of PCP use on PFAS concentrations in pregnant and lactating populations. Objective We investigated associations between PCP use and PFAS concentrations in prenatal plasma and human milk. Methods We leveraged the Maternal-Infant Research on Environmental Chemicals (MIREC) Study to evaluate the contribution of PCP use on PFAS concentrations in prenatal plasma (6 to 13 weeks’ gestation; n = 1,940) and human-milk (2 to 10 weeks’ postpartum; n = 664). Participants reported frequency of use across 8 PCP categories during the 1st and 3rd trimesters, 1 to 2 days postpartum, and 2 to 10 weeks’ postpartum. We used adjusted linear regression models to quantify percent differences and corresponding 95 % confidence intervals. Results In 1st trimester pregnant people, we found higher use of nailcare products (≥once a week vs. never: perfluorooctanoic acid (PFOA): 21 % [9.7 %, 32 %]; perfluorooctane-sulfonic acid (PFOS): 11 % [0.3 %, 23 %]), fragrances (daily vs. never: PFOA: 14 % [7.8 %, 21 %]; PFOS: 7.8 % [1.3 %, 15 %]), makeup (daily vs. never: PFOA: 14 % [5.8 %, 23 %]), hair dyes (never vs. 1-2 times during pregnancy: PFOA: 8.3 % [2.4 %, 15 %]), and hair sprays or gels (daily vs. never: PFOA: 12 % [5.0 %, 19 %], PFOS: 7.1 % [0.2 %, 15 %]) were associated with higher plasma PFAS concentrations. Similar results were observed for 3rd trimester PCP use and 2 to 10 weeks’ postpartum human-milk PFAS concentrations. In addition, we also found that people using colored-permanent dye 1 to 2 days postpartum had higher Sm-PFOS (18 % [2.7 %, 35 %]), PFOA (16 % [4.3 %, 29 %]), and perfluorononanoic acid (17 % [3.6 %, 33 %]) postpartum human-milk concentrations. Conclusions Our results show that PCP use may be a modifiable source of PFAS exposure in pregnant and lactating populations. These results along with growing scientific evidence can help inform PFAS regulation and guide individual choices to reduce PFAS exposure.