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BACKGROUND: Federal housing assistance is an important policy tool to ensure housing security for low-income households. Less is known about its impact on residential environmental exposures, particularly lead. OBJECTIVES: We conducted a quasi-experimental study to investigate the association between federal housing assistance and blood lead levels (BLLs) in a nationally representative US sample age 6 y and older eligible for housing assistance. METHODS: We used the 1999-2018 National Health and Nutrition Examination Survey (NHANES) linked with US Department of Housing and Urban Development (HUD) administrative records to assess BLLs of NHANES participants with concurrent HUD housing assistance (i.e., current recipients, 푛=3,071) and those receiving assistance within 2 y after the survey (i.e., pseudo-waitlist recipients, 푛=1,235). We estimated BLL least squares geometric means (LSGMs), odds ratio (OR) for BLL ≥3.5 μg/dL, and percent differences in LSGMs by HUD housing assistance status adjusting for age, sex, family income-to-poverty ratio, education, country of birth, race/ethnicity, region, and survey year. We also examined effect modification using interaction terms and stratified analyses by program type [i.e., public housing, multifamily, housing choice vouchers (HCV)], and race/ethnicity. RESULTS: Current HUD recipients had a significantly lower LSGM [1.07 μg/dL; 95% confidence interval (CI): 1.02, 1.12] than pseudo-waitlist recipients (1.21 μg/dL; 95% CI: 1.14, 1.28), with an adjusted OR of 0.60 (95% CI: 0.42, 0.87) for BLL ≥3.5 μg/dL. Some effect modification were observed: The protective association of HUD assistance on BLL was strongest among public housing (-19.5% LSGM; 95% CI: -27.5%, -10.7%), multifamily (-12.5% LSGM; 95% CI: -20.7%, -3.5%), and non-Hispanic White (-20:6% LSGM; 95% CI: -29.8%, -10.3%) recipients. It was weaker to null among HCV (-5.7% LSGM; 95% CI: -12.7, 1.7%), non-Hispanic Black (-1.6% LSGM; 95% CI: -8.1%, 5.4%), and Mexican American (-12.5% LSGM; 95% CI: -31.9%, 12.5%) recipients. DISCUSSION: Our research underscores the importance of social-structural determinants like federal housing assistance in providing affordable, stable, and healthy housing to very low-income households. More attention is needed to ensure housing quality and racial equity across HUD's three major housing assistance programs. [ABSTRACT FROM AUTHOR]

BACKGROUND: Phthalate exposures are ubiquitous during pregnancy and may contribute to racial and ethnic disparities in preterm birth. OBJECTIVES: We investigated race and ethnicity in the relationship between biomarkers of phthalate exposure and preterm birth by examining: a) how hypothetical reductions in racial and ethnic disparities in phthalate metabolites might reduce the probability of preterm birth; and b) exposure–response models stratified by race and ethnicity. METHODS: We pooled individual-level data on 6,045 pregnancies from 16 U.S. cohorts. We investigated covariate-adjusted differences in nine urinary phthalate metabolite concentrations by race and ethnicity [non-Hispanic White (White, 43%), non-Hispanic Black (Black, 13%), Hispanic/Latina (38%), and Asian/Pacific Islander (3%)]. Using g-computation, we estimated changes in the probability of preterm birth under hypothetical interventions to eliminate disparities in levels of urinary phthalate metabolites by proportionally lowering average concentrations in Black and Hispanic/ Latina participants to be approximately equal to the averages in White participants. We also used race and ethnicity-stratified logistic regression to characterize associations between phthalate metabolites and preterm birth. RESULTS: In comparison with concentrations among White participants, adjusted mean phthalate metabolite concentrations were consistently higher among Black and Hispanic/Latina participants by 23%–148% and 4%–94%, respectively. Asian/Pacific Islander participants had metabolite levels that were similar to those of White participants. Hypothetical interventions to reduce disparities in metabolite mixtures were associated with lower probabilities of preterm birth for Black [13% relative reduction; 95% confidence interval (CI): -34%, 8.6%] and Hispanic/Latina (9% relative reduction; 95% CI: -19%, 0.8%) participants. Odds ratios for preterm birth in association with phthalate metabolites demonstrated heterogeneity by race and ethnicity for two individual metabolites (mono-n-butyl and monoisobutyl phthalate), with positive associations that were larger in magnitude observed among Black or Hispanic/Latina participants. CONCLUSIONS: Phthalate metabolite concentrations differed substantially by race and ethnicity. Our results show hypothetical interventions to reduce population-level racial and ethnic disparities in biomarkers of phthalate exposure could potentially reduce the probability of preterm birth. [ABSTRACT FROM AUTHOR]

Information technology improves reliability, innovation, and efficiency in the medical care sector by assisting in coming up with electronic health records. Looking into the interoperability of software and databases is relevant from the perspective of electronic health records. The standardization of processes in the European Union and the United States is diverse, which makes it all the more important to discuss open standards. Software systems create patient-centric medical care services and a platform for management. Thus, they facilitate the formation of functional health information networks and the exchange of information. Therefore, this improves the value proposition for all stakeholders involved. Open-source standards have been found to be developed independently of any single party. They do not have any legal or technical closest that prevent any party to use them. Similarly, they do not have extensions or components with a dependency or being based on preparation standards. Additionally, they are available for full public assessment without any form of constraints. This paper discusses these open standards and how best they have been deployed in the United States and the European Union -- understanding that advantages and disadvantages of open standards are also imperative. [ABSTRACT FROM AUTHOR]

Background: Leukocyte telomere length (LTL) is a putative biological marker of immune system age, and there are demonstrated associations between LTL and cardiovascular disease. This may be due in part to the relationship of LTL with other biomarkers associated with cardiovascular disease risk. However, the strength of associations between LTL and adiposity, metabolic, proinflammatory, and cardiovascular biomarkers has not been systematically evaluated in a United States nationally representative population.Methods and Findings: We examined associations between LTL and 17 cardiovascular biomarkers, including lipoproteins, blood sugar, circulatory pressure, proinflammatory markers, kidney function, and adiposity measures, in adults ages 20 to 84 from the cross-sectional US nationally representative 1999-2002 National Health and Nutrition Examination Survey (NHANES) (n = 7,252), statistically adjusting for immune cell type distributions. We also examine whether these associations differed systematically by age, race/ethnicity, gender, education, and income. We found that a one unit difference in the following biomarkers were associated with kilobase pair differences in LTL: BMI -0.00478 (95% CI -0.00749--0.00206), waist circumference -0.00211 (95% CI -0.00325--0.000969), percentage of body fat -0.00516 (95% CI -0.00761--0.0027), high density lipoprotein (HDL) cholesterol 0.00179 (95% CI 0.000571-0.00301), triglycerides -0.000285 (95% CI -0.000555--0.0000158), pulse rate -0.00194 (95% CI -0.00317--0.000705), C-reactive protein -0.0363 (95% CI 0.0601--0.0124), cystatin C -0.0391 (95% CI -0.0772--0.00107). When using clinical cut-points we additionally found associations between LTL and insulin resistance -0.0412 (95% CI -0.0685--0.0139), systolic blood pressure 0.0455 (95% CI 0.00137-0.0897), and diastolic blood pressure -0.0674 (95% CI -0.126--0.00889). These associations were 10%-15% greater without controlling for leukocyte cell types. There were very few differences in the associations by age, race/ethnicity, gender, education, or income. Our findings are relevant to the relationships between these cardiovascular biomarkers in the general population but not to cardiovascular disease as a clinical outcome.Conclusions: LTL is most strongly associated with adiposity, but is also associated with biomarkers across several physiological systems. LTL may thus be a predictor of cardiovascular disease through its association with multiple risk factors that are physiologically correlated with risk for development of cardiovascular disease. Our results are consistent with LTL being a biomarker of cardiovascular aging through established physiological mechanisms. [ABSTRACT FROM AUTHOR]

BACKGROUND: Phthalates and bisphenol A (BPA) are widely used industrial chemicals that may adversely impact human health. Human exposure is ubiquitous and can occur through diet, including consumption of processed or packaged food. OBJECTIVE: To examine associations between recent fast food intake and BPA and urinary metabolites of di(2-ethylhexyl) phthalate ^DEHPm) and diisononyl phthalate (DiNPm) among the U.S. population. METHODS: We combined data on 8,877 participants from the National Health and Nutrition Examination Survey (NHANES 2003-2010). Using 24-hr dietary recall data, we quantified: a) fast food intake [percent of total energy intake (TEI) from fast food]; b) fast food-derived fat intake (percent of TEI from fat in fast food); and c) fast food intake by food group (dairy, eggs, grains, meat, and other). We examined associations between dietary exposures and urinary chemical concentrations using multivariate linear regression. RESULTS: We observed evidence of a positive, dose -- response relationship between fast food intake and exposure to phthalates (^-trend < 0.0001) but not BPA; participants with high consumption (≥ 34.9% TEI from fast food) had 23.8% (95% CI: 11.9%, 36.9%) and 39.0% (95% CI: 21.9%, 58.5%) higher levels of ΣDEHPm and DiNPm, respectively, than nonconsumers. Fast food-derived fat intake was also positively associated with ΣDEHPm and DiNPm (^-trend < 0.0001). After adjusting for other food groups, ΣDEHPm was associated with grain and other intake, and DiNPm was associated with meat and grain intake. CONCLUSION: Fast food may be a source of exposure to DEHP and DiNP. These results, if confirmed, could inform individual and regulatory exposure reduction strategies. CITATION: Zota AR, Phillips CA, Mitro SD. 2016. Recent fast food consumption and bisphenol A and phthalates exposures among the U.S. population in NHANES, 2003-2010. Environ Health Perspect 124:1521-1528; http://dx.doi.org/10.1289/ehp.1510803 [ABSTRACT FROM AUTHOR]

BACKGROUND: Exposure to persistent organic pollutants (POPs) such as dioxins, furans, and polychlorinated biphenyls (PCBs) may influence leukocyte telomere length (LTL), a biomarker associated with chronic disease. In vitro research suggests dioxins may bind to the aryl hydrocarbon receptor (AhR) and induce telomerase activity, which elongates LTL. However, few epidemiologic studies have investigated associations between POPs and LTL. OBJECTIVES: We examined the association between 18 PCBs, 7 dioxins, and 9 furans and LTL among 1,330 U.S. adults from NHANES 2001-2002. METHODS: We created three summed POP metrics based on toxic equivalency factor (TEF), a potency measure including affinity for the AhR: a) non-dioxin-like PCBs (composed of 10 non-dioxin-like PCBs; no AhR affinity and no TEF); b) non-ortho PCBs (composed of 2 non-ortho-substituted PCBs with high TEFs); and c) toxic equivalency (TEQ) (composed of 7 dioxins, 9 furans, 2 non-ortho-substituted PCBs, and 6 mono-ortho-substituted PCBs; weighted by TEF). We tested the association between each metric and LTL using linear regression, adjusting for demographics, blood cell count and distribution, and another metric with a different TEF (i.e., non-ortho PCBs and TEQ adjusted for non-dioxin-like PCBs; non-dioxin-like PCBs adjusted for non-ortho PCBs). RESULTS: In adjusted models, each doubling of serum concentrations of non-ortho PCBs and TEQ was associated with 3.74% (95% CI: 2.10, 5.40) and 5.29% (95% CI: 1.66, 9.05) longer LTLs, respectively. Compared with the lowest quartile, the highest quartile of exposure was associated with 9.16% (95% CI: 2.96, 15.73) and 7.84% (95% CI: -0.53, 16.92) longer LTLs, respectively. Non-dioxin-like PCBs were not associated with LTL. CONCLUSIONS: POPs with high TEFs and AhR affinity were associated with longer LTL. Because many dioxin-associated cancers are also associated with longer LTL, these results may provide insight into the mechanisms underlying PCB- and dioxin-related carcinogenesis. [ABSTRACT FROM AUTHOR]

Cadmium and lead are ubiquitous environmental contaminants that might increase risks of cardiovascular disease and other aging-related diseases, but their relationships with leukocyte telomere length (LTL), a marker of cellular aging, are poorly understood. In experimental studies, they have been shown to induce telomere shortening, but no epidemiologic study to date has examined their associations with LTL in the general population. We examined associations of blood lead and cadmium (n = 6,796) and urine cadmium (n = 2,093) levels with LTL among a nationally representative sample of US adults from the National Health and Nutrition Examination Survey (1999–2002). The study population geometric mean concentrations were 1.67 µg/dL (95% confidence interval (CI): 1.63, 1.70) for blood lead, 0.44 µg/L (95% CI: 0.42, 0.47) for blood cadmium, and 0.28 µg/L (95% CI: 0.27, 0.30) for urine cadmium. After adjustment for potential confounders, the highest (versus lowest) quartiles of blood and urine cadmium were associated with −5.54% (95% CI: −8.70, −2.37) and −4.50% (95% CI: −8.79, −0.20) shorter LTLs, respectively, with evidence of dose-response relationship (P for trend < 0.05). There was no association between blood lead concentration and LTL. These findings provide further evidence of physiological impacts of cadmium at environmental levels and might provide insight into biological pathways underlying cadmium toxicity and chronic disease risks. [ABSTRACT FROM PUBLISHER]

Background: Phthalates are ubiquitous environmental contaminants. Because of potential adverse effects on human health, butylbenzyl phthalate [BBzP; metabolite, monobenzyl phthalate (MBzP)], di-n-butyl phthalate [DnBP; metabolite, mono-n-butyl phthalate (MnBP)], and di(2-ethylhexyl) phthalate (DEHP) are being replaced by substitutes including other phthalates; however, little is known about consequent trends in population-level exposures. Objective: We examined temporal trends in urinary concentrations of phthalate metabolites in the general U.S. population and whether trends vary by sociodemographic characteristics. Methods: We combined data on 11 phthalate metabolites for 11,071 participants from five cycles of the National Health and Nutrition Examination Survey (2001–2010). Percent changes and least square geometric means (LSGMs) were calculated from multivariate regression models. Results: LSGM concentrations of monoethyl phthalate, MnBP, MBzP, and ΣDEHP metabolites decreased between 2001–2002 and 2009–2010 [percent change (95% CI): –42% (–49, –34); –17% (–23, –9); –32% (–39, –23) and –37% (–46, –26), respectively]. In contrast, LSGM concentrations of monoisobutyl phthalate, mono(3-carboxypropyl) phthalate (MCPP), monocarboxyoctyl phthalate, and monocarboxynonyl phthalate (MCNP) increased over the study period [percent change (95% CI): 206% (178, 236); 25% (8, 45); 149% (102, 207); and 15% (1, 30), respectively]. Trends varied by subpopulations for certain phthalates. For example, LSGM concentrations of ΣDEHP metabolites, MCPP, and MCNP were higher in children than adults, but the gap between groups narrowed over time (pinteraction < 0.01). Conclusions: Exposure of the U.S. population to phthalates has changed in the last decade. Data gaps make it difficult to explain trends, but legislative activity and advocacy campaigns by nongovernmental organizations may play a role in changing trends. [ABSTRACT FROM AUTHOR]

Background: Scientists and regulators have sought to understand whether and how physiologic dysregulation due to chronic stress exposure may enhance vulnerability to the adverse health effects of toxicant exposures. We conducted a cross-sectional study to determine whether allostatic load (AL), a composite measure of physiologic response to chronic exposure to stress, amplifies the effect of lead exposure on blood pressure among middle-aged adults. Methods: We analyzed associations between blood lead levels and blood pressure in a nationally representative sample of 8,194 U.S. adults (aged 40-65 years) participating in the National Health and Nutritional Examination Survey, 1999--2008. Outcomes were elevated systolic (⩾ 140 mm Hg) and diastolic (⩾ 90 mm Hg) blood pressure. AL was defined as the aggregate score of seven components, reflecting dysregulation of the cardiovascular, inflammatory, and endocrine systems. Results: Logistic regression models showed a linear dose-response relationship for quintiles of blood lead and elevated systolic blood pressure in the high AL group (p = 0.03) but not the low AL group (p = 0.24). Similarly, the relationship between lead exposure and elevated diastolic blood pressure was stronger among the high AL group than the low AL group. Within the high AL group, the fourth and fifth quintiles had significantly elevated odds of elevated blood pressure compared to lowest quintile [OR = 1.92, (95% CI, 1.07, 3.47) and OR =2.28 (95% CI, 1.33, 3.91), respectively]. In the low AL group, none of the quintile effects were significantly different than the referent group although there was evidence of a linear trend (p =0.03). The lead by AL interaction term was not statistically significant for either systolic or diastolic blood pressure models. Conclusions: Results suggest that higher AL may amplify the adverse effects of lead on blood pressure. Future research should assess the implications of cumulative exposures to environmental and social stressors for regulatory decision-making. [ABSTRACT FROM AUTHOR]

Objectives. The indoor environment has not been fully incorporated into the environmental justice dialogue. To inform strategies to reduce disparities, we developed a framework to identify the individual and place-based drivers of indoor environment quality. Methods. We reviewed empirical evidence of socioeconomic disparities in indoor exposures and key determinants of these exposures for air pollutants, lead, allergens, and semivolatile organic compounds. We also used an indoor air quality model applied to multifamily housing to illustrate how nitrogen dioxide (NO2) and fine particulate matter (PM2.5) vary as a function of factors known to be influenced by socioeconomic status. Results. Indoor concentrations of multiple pollutants are elevated in low socioeconomic status households. Differences in these exposures are driven by the combined influences of indoor sources, outdoor sources, physical structures, and residential activity patterns. Simulation models confirmed indoor sources' importance in determining indoor NO2 and PM2.5 exposures and showed the influence of household-specific determinants. Conclusions. Both theoretical models and empirical evidence emphasized that disparities in indoor environmental exposure can be significant. Understanding key determinants of multiple indoor exposures can aid in developing policies to reduce these disparities. [ABSTRACT FROM AUTHOR]

BacKground: Exposure to chemicals during fetal development can increase the risk of adverse health effects, and while biomonitoring studies suggest pregnant women are exposed to chemicals, little is known about the extent of multiple chemicals exposures among pregnant women in the United States. Objective: We analyzed biomonitoring data from the National Health and Nutritional Examination Survey (NHANES) to characterize both individual and multiple chemical exposures in U.S. pregnant women. Methods: We analyzed data for 163 chemical analytes in 12 chemical classes for subsamples of 268 pregnant women from NHANES 2003-2004, a nationally representative sample of the U.S. population. For each chemical analyte, we calculated descriptive statistics. We calculated the number of chemicals detected within the following chemical classes: polybrominated diphenyl ethers (PBDEs), perfluorinated compounds (PFCs), organochlorine pesticides, and phthalates and across multiple chemical classes. We compared chemical analyte concentrations for pregnant and nonpregnant women using least-squares geometric means, adjusting for demographic and physiological covariates. results: The percentage of pregnant women with detectable levels of an individual chemical ranged from 0 to 100%. Certain polychlorinated biphenyls, organochlorine pesticides, PFCs, phenols, PBDEs, phthalates, polycyclic aromatic hydrocarbons, and perchlorate were detected in 99-100% of pregnant women. The median number of detected chemicals by chemical class ranged from 4 of 12 PFCs to 9 of 13 phthalates. Across chemical classes, median number ranged from 8 of 17 chemi­cal analytes to 50 of 71 chemical analytes. We found, generally, that levels in pregnant women were similar to or lower than levels in nonpregnant women; adjustment for covariates tended to increase levels in pregnant women compared with nonpregnant women. conclusions: Pregnant women in the U.S. are exposed to multiple chemicals. Further efforts are warranted to understand sources of exposure and implications for policy making. [ABSTRACT FROM AUTHOR]

Atmospheric dispersion of particles from mine waste is potentially an important route of human exposure to metals in communities close to active and abandoned mining areas. This study assessed sources of mass and metal concentrations in two size fractions of respirable particles using positive matrix factorization (U.S. Environmental Protection Agency [EPA] PMF 3.0). Weekly integrated samples of particulate matter (PM) 10 μm in aerodynamic diameter or less (PM10) and fine PM (PM2.5, or PM <2.5 μm in aerodynamic diameter) were collected at three monitoring sites, varying distances (0.5-20 km) from mine waste piles, for 58 consecutive weeks in a former lead (Pb) and zinc (Zn) mining region. Mean mass concentrations varied significantly across sites for coarse PM (PM10-PM2.5) but not PM2.5 particles. Concentrations of Pb and Zn significantly decreased with increasing distance from the mine waste piles in PM10-PM2.5 (P < 0.0001) and PM2.5 (P < 0.0005) fractions. Source apportionment analyses deduced five sources contributing to PM2.5 (mobile source combustion, secondary sulfates, mine waste, crustal/soil, and a source rich in calcium [Ca]) and three sources for the coarse fraction (mine waste, crustal/soil, and a Ca-rich source). In the PM2.5 fraction, mine waste contributed 1-6% of the overall mass, 40% of Pb, and 63% of Zn. Mine waste impacts were more apparent in the PM10-PM2.5 fraction and contributed 4-39% of total mass, 88% of Pb, and 97% of Zn. Percent contribution of mine waste varied significantly across sites (P < 0.0001) for both size fractions, with highest contributions in the site closest to the mine waste piles. Seasonality, wind direction, and concentrations of the Ca-rich source were also associated with levels of ambient aerosols from the mine waste source. Scanning electron microscopy results indicated that the PMF-identified mine waste source is mainly composed of Zn-Pb agglomerates on crustal particles in the PM10-PM2.5 fraction. In conclusion, the differential impacts of mine waste on respirable particles by size fraction and location should be considered in future exposure evaluations. [ABSTRACT FROM AUTHOR]

Studies show higher house dust and body burden levels of PBDE flame retardants in North America than Europe; but little is known about exposure variation within North America, where California's furniture flammability standard affects PBDE use. We compared dust samples from 49 homes in two California communities with 120 Massachusetts homes and with other published studies. Dust concentrations [median (range) ng/g} in California homes of BDE-47, -99, and -100 were 2700 (112-107 000), 3800 (102-170 000), and 684 (

Indoor dust is a reservoir for commercial consumer product chemicals, including many compounds with known or suspected health effects. However, most dust exposure studies measure few chemicals in small samples. We systematically searched the U.S. indoor dust literature on phthalates, replacement flame retardants (RFRs), perfluoroalkyl substances (PFASs), synthetic fragrances, and environmental phenols and estimated pooled geometric means (GMs) and 95% confidence intervals for 45 chemicals measured in =3 data sets. In order to rank and contextualize these results, we used the pooled GMs to calculate residential intake from dust ingestion, inhalation, and dermal uptake from air, and then identified hazard traits from the Safer Consumer Products Candidate Chemical List. Our results indicate that U.S. indoor dust consistently contains chemicals from multiple classes. Phthalates occurred in the highest concentrations, followed by phenols, RFRs, fragrance, and PFASs. Several phthalates and RFRs had the highest residential intakes. We also found that many chemicals in dust share hazard traits such as reproductive and endocrine toxicity. We offer recommendations to maximize comparability of studies and advance indoor exposure science. This information is critical in shaping future exposure and health studies, especially related to cumulative exposures, and in providing evidence for intervention development and public policy. [ABSTRACT FROM AUTHOR]

[Display omitted] • Hypertensive disorders of pregnancy (HDP) cause substantial morbidity and mortality. • PFAS exposure may adversely affect cardiometabolic health during pregnancy. • We estimated associations of plasma PFAS and PFAS mixtures with HDP and BP. • PFAS were associated with higher odds of gestational hypertension, not preeclampsia. • PFAS were positively associated with mean 2nd and 3rd trimester diastolic BP. Hypertensive disorders of pregnancy (HDP), defined here as hypertensive disorders with onset in pregnancy (i.e., gestational hypertension, preeclampsia, and preeclampsia superimposed on chronic hypertension), affect up to 10% of pregnancies in the United States and are associated with substantial maternal and neonatal morbidity and mortality. Per- and polyfluoroalkyl substances (PFAS) are associated with adverse cardiometabolic outcomes during pregnancy, but associations between PFAS and HDP are inconsistent and joint effects of PFAS mixtures have not been evaluated. We studied 1,558 pregnant individuals from the Project Viva cohort, recruited during 1999–2002. We quantified concentrations of eight PFAS in plasma samples (median 9.7 weeks of gestation). Using clinical records, we calculated trimester-specific mean systolic (SBP) and diastolic (DBP) blood pressure and categorized HDP status [no HDP (normotensive & chronic hypertension), gestational hypertension, preeclampsia]. We estimated associations of individual PFAS with HDP using multinomial logistic regression and estimated associations with blood pressure using linear regression. We used Bayesian kernel machine regression (BKMR) and quantile g-computation to assess joint effects of the PFAS mixture on HDP and blood pressure measures. Four percent of participants developed preeclampsia and 7% developed gestational hypertension. We observed higher odds of gestational hypertension, but not preeclampsia, per doubling of perfluorooctanoate (PFOA) [OR = 1.51 (95% confidence interval: 1.12, 2.03)], perfluorooctane sulfonate (PFOS) [OR = 1.38 (1.04, 1.82)], and perfluorohexane sulfonate [OR = 1.28 (1.06, 1.54)] concentrations. We observed higher mean DBP per doubling of PFOA [2nd trimester (T2): 0.39 mmHg (−0.01, 0.78); 3rd trimester (T3): 0.56 mmHg (0.14, 0.98)] and PFOS [T2: 0.46 mmHg (0.11, 0.82); T3: 0.43 mmHg (0.05, 0.80)]. The PFAS mixture was positively associated with odds of gestational hypertension [75th vs. 50th percentile: OR = 1.14 (95% credible interval:1.03, 1.25), BKMR] and mean DBP [T2 = 0.17 mmHg (−0.06, 0.40); T3 = 0.22 mmHg (−0.03, 0.48), BKMR]. These findings suggest that exposure to certain PFAS may increase the odds of gestational hypertension during pregnancy, with potential implications for subsequent maternal and child health outcomes. [ABSTRACT FROM AUTHOR]