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Intersectionality is a critical theoretical framework that emphasizes the influence of intersecting systems of oppression on the lived experiences of people marginalized by inequity. Although applications of intersectionality are increasing in public health, this framework is absent in environmental health, which has instead focused on the exposome, a paradigm that considers the totality of an individual's environmental exposures across the life course. Despite advancements in the biological complexity of exposome models, they continue to fall short in addressing health inequities. Therefore, we highlight the need for integrating intersectionality into the exposome. We introduce key concepts and tools for environmental health scientists interested in operationalizing intersectionality in exposome studies and discuss examples of this innovative approach from our work on racial inequities in uterine fibroids. Our case studies illustrate how interlocking systems of racism and sexism may affect Black women's exposure to environmental chemicals, their epigenetic regulation of uterine fibroids, and their clinical care. Because health relies on biological and social–structural determinants and varies across different intersectional positions, our proposed framework may be a promising approach for understanding environmental health inequities and furthering social justice. [ABSTRACT FROM AUTHOR]

Phthalates are associated with multiple, adverse reproductive outcomes including increased risk of uterine leiomyoma (fibroids). Phthalates can interact with epigenetic modifications including microRNAs (miRNAs), which help regulate processes crucial to fibroid pathogenesis. However, no prior study has examined the influence of phthalates on miRNA expression in fibroid tumors. We conducted a preliminary, cross-sectional study to examine the associations between phthalate exposures and miRNA expression levels in fibroid tumors and to explore potential effect modification by race/ethnicity. We quantified expression levels of 754 miRNAs in fibroid tumor samples and analyzed spot urine samples for phthalate metabolites collected from 45 pre-menopausal women undergoing surgery for fibroid treatment at an academic hospital. Associations between miRNA levels in fibroids and phthalate biomarkers were evaluated using linear regression adjusting for age, race/ethnicity, and body mass index (BMI). Statistical tests were adjusted for multiple comparisons. We also performed in silico Ingenuity Pathway Analysis to identify the biological pathways that are regulated by phthalate-associated miRNAs. Mono-hydroxybutyl phthalate and mono(2-ethyl-5-hydroxyhexyl) phthalate were positively associated with miR-10a-5p (β = 0.76, 95% CI = [0.40, 1.11]) and miR-577 (β = 1.06, 95% CI = [0.53, 1.59]), respectively. A total of 8 phthalate-miRNA associations varied by race/ethnicity (qinteraction < 0.10). Pathway analysis revealed that mRNA gene targets of phthalate-associated miRNAs were significantly associated with multiple fibroid-related processes including angiogenesis, apoptosis, and proliferation of connective tissues. Collectively, these data suggest that exposures to some phthalates are associated with miRNA in fibroids, and that associations may vary by race/ethnicity. Validation of these findings may provide insight into mechanisms underlying associations between phthalates and fibroids and contribute to novel hypotheses regarding racial/ethnic disparities in fibroids. [ABSTRACT FROM AUTHOR]

Objectives: To examine the association between phthalate exposure and two measures of uterine fibroid burden: diameter of largest fibroid and uterine volume.Design: Pilot, cross-sectional study.Setting: Academic medical center.Patient(s): Fifty-seven premenopausal women undergoing either hysterectomy or myomectomy for fibroids.Intervention(s): None.Main Outcome Measure(s): The diameter of the largest fibroid and uterine dimensions were abstracted from medical records. Spot urine samples were analyzed for 14 phthalate biomarkers using mass spectrometry. We estimated associations between fibroid outcomes and individual phthalate metabolites, sum of di(2-ethylhexyl) phthalate metabolites (∑DEHP), and a weighted sum of anti-androgenic phthalate metabolites (∑AA Phthalates) using linear regression, adjusting for age, race/ethnicity, and body mass index. Fibroid outcomes were also examined dichotomously (divided at the median) using logistic regression.Results: Most women were of black ethnicity, overweight or obese, and college educated. In multivariable models, higher levels of mono-hydroxyisobutyl phthalate, monocarboxyoctyl phthalate, monocarboxynonyl phthalate, mono(2-ethylhexyl) phthalate, mono(2-ethyl-5-hydroxyhexyl phthalate) (MEHHP), mono(2-ethyl-5-oxohexyl) phthalate (MEOHP), and mono(2-ethyl-5-carboxypentyl) phthalate (MECPP), ∑DEHP, and ∑AA Phthalates were positively associated with uterine volume. Associations were most pronounced for individual DEHP metabolites (MEHHP, MEOHP, MECPP), ∑DEHP, and ∑AA Phthalates. For example, a doubling in ∑DEHP and ∑AA Phthalates was associated with 33.2% (95% confidence interval 6.6-66.5) and 26.8% (95% confidence interval 2.2-57.4) increase in uterine volume, respectively. There were few associations between phthalate biomarkers and fibroid size.Conclusions: Exposure to some phthalate biomarkers was positively associated with uterine volume, which further supports the hypothesis that phthalate exposures may be associated with fibroid outcomes. Additional studies are needed to confirm these relationships. [ABSTRACT FROM AUTHOR]

Background Endocrine-disrupting chemicals (EDCs) can target immune and metabolic pathways. However, few epidemiologic studies have examined the influence of EDCs on measures of inflammation and cellular aging during pregnancy and postpartum. Objective We investigated associations between prenatal exposures to polybrominated diphenyl ethers (PBDEs), hydroxylated PBDE metabolites (OH-PBDEs), polychlorinated biphenyls (PCBs), and per- and polyfluorochemicals (PFASs) with repeated biomarker measurements of inflammation and cellular aging in women during pregnancy and the postpartum period. Methodology Overweight or obese pregnant women were recruited from the San Francisco Bay area (n = 103) during their first or second trimester of pregnancy. Blood samples were collected from participants at baseline (median 16 weeks gestation) and at three and nine months postpartum. Serum concentrations of PBDEs, OH-PBDEs, PCBs, and PFASs were measured at baseline. Inflammation biomarkers (interleukin 6 [IL-6], interleukin 10 [IL-10], and tumor necrosis factor [TNF-α]) and leukocyte telomere length (LTL), a biomarker of cellular aging, were measured at all three time points. Associations between serum chemical concentrations and repeated measures of IL-6, IL-10, TNF-α, and LTL were examined using linear mixed models. We also examined the potential for effect modification by time (visit) and obesity. Results In adjusted models, we observed positive relationships between PBDEs and pro-inflammatory cytokines (IL-6 and TNF-α). A doubling in ∑PBDEs was associated with a 15.26% (95% CI 1.24, 31.22) and 3.74% (95% CI −0.19, 7.82) increase in IL-6 and TNF-α, respectively. Positive associations were also observed for PFASs and IL-6. A two-fold increase in ∑PFASs was associated with a 20.87% (95% CI 3.46, 41.22) increase in IL-6. 5-OHBDE-47 was inversely associated with anti-inflammatory cytokine IL-10. Some EDC-outcome associations, including those of PBDEs with TNF-α, were stronger during pregnancy (compared to three or nine months postpartum) and among obese (compared to overweight) women (p-interaction <0.05). Conclusions These findings suggest that exposure to specific EDCs is associated with increased inflammation among women during pregnancy and the postpartum period. Future studies should replicate these findings in additional study populations and examine the implications of these associations for maternal and child health. [ABSTRACT FROM AUTHOR]

Polybrominated diphenyl ethers (PBDEs) are brominated flame retardants. Technical mixtures PentaBDE and OctaBDE were phased out in 2004 through voluntary and regulatory actions with DecaBDE remaining in limited use until 2013. Biomonitoring studies have shown widespread presence of PBDEs in the US and worldwide population. While some studies suggest that human serum concentrations are declining over time, it is unclear whether this trend will continue. Our objective was to examine temporal trends of PentaBDEs and their hydroxylated metabolites (OH-PBDEs) between 2008 and 2014 in populations of ethnically diverse, pregnant women residing in Northern California (n = 111). Serum samples were collected and analyzed by high resolution mass spectrometry for five PentaBDE congeners and two OH-PBDEs. We found widespread exposures in participants from all three time points (2008/09, 2011/12, 2014). Temporal patterns varied substantially by congener. BDE-47, -99 and the OH-PBDEs decreased between 2008/09-2011/12 but plateaued between 2011/12-2014. In contrast, BDE-100 decreased across all years, BDE-153 decreased in the latter years, and BDE-28 decreased initially and then increased. These findings indicate that while policies to remove PBDEs from the marketplace have successfully lead to declines in exposures to some PBDE congeners, human exposures to these legacy pollutants could plateau and remain ubiquitous in human populations. [ABSTRACT FROM AUTHOR]

Background Human fetal exposures to polybrominated diphenyl ethers (PBDEs) and their metabolites (OH-PBDEs) are unique from adults, and in combination with a different metabolic profile, may make fetal development more sensitive to adverse health outcomes from these exposures. However, we lack data to characterize human fetal PBDE exposures and the metabolic factors that can influence these exposures. Objective We examined differences between 2nd trimester maternal and fetal exposures to PBDEs and OH-PBDEs. We also characterized fetal cytochrome P450 (CYP) mRNA expression and its associations with PBDE exposures. Methods We collected paired samples of maternal serum and fetal liver ( n = 86) with a subset having matched placenta ( n = 50). We measured PBDEs, OH-PBDEs, and mRNA expression of CYP genes (e.g. CYP1A1, -2E1, -2J2, -2C9) in all samples. As a sensitivity analysis, we measured PBDEs and OH-PBDEs in umbilical cord serum from a subset ( n = 22). Results BDE-47 was detected in ≥ 96% of all tissues. Unadjusted ∑PBDEs concentrations were highest in fetal liver (geometric mean (GM) = 0.72 ng/g), whereas lipid-adjusted concentrations were highest in cord serum (111.12 ng/g lipid). In both cases, fetal concentrations were approximately two times higher than maternal serum levels (GM = 0.33 ng/g or 48.75 ng/g lipid). ΣOH-PBDEs were highest in maternal and cord sera and 20–200 times lower than PBDE concentrations. In regression models, maternal BDE-47 explained more of the model variance of liver than of placenta BDE-47 concentrations (adjusted R 2 = 0.79 vs 0.48, respectively). In adjusted logistic regression models, ∑PBDEs were positively associated with expression of CYP2E1 and -2J2 (placenta), and -1A1 (liver) ( p < 0.05). Conclusion Our findings suggest that under normal conditions of mid-gestation, the human fetus is directly exposed to concentrations of PBDEs that may be higher than previously estimated based on maternal serum and that these exposures are associated with the expression of mRNAs coding for CYP enzymes. These results will help frame and interpret findings from studies that use maternal or cord blood as proxy measures of fetal exposures, and will inform the molecular pathways by which PBDEs affect human health. [ABSTRACT FROM AUTHOR]

Phthalates are ubiquitous chemicals linked to hormonal disruptions that affect reproduction and development. Multiple antiandrogenic phthalates exposure during fetal development can have greater impacts than individual exposure; thus, the National Academy of Sciences (NAS) recommends them for cumulative assessment. Using National Health and Nutrition Examination Survey data (NHANES, 2001-2012), we developed a potency-weighted sum of daily intake (∑androgen-disruptor; μg/kg/day) of di-n-butyl phthalate (DnBP), diisobutyl phthalate (DiBP), butyl benzyl phthalate (BBzP), and di(2-ethylhexyl) phthalate (DEHP) based on NAS recommendations, and included diethyl phthalate (DEP) and diisononyl phthalate (DiNP) in additional metrics (2005-2012). We compared racial/ethnic differences in ∑androgen-disruptor among 2842 reproductive-aged women. In sensitivity analyses, we assessed the influence of potency assumptions, alternate urine dilution adjustment methods, and weighting phthalate metabolites directly rather than daily intake estimates of parent compounds. We found that DEHP contributed most to ∑androgen-disruptor (48-64%), and that ∑androgen-disruptor decreased over time. Black women generally had higher cumulative exposures than white women, although the magnitude and precision of the difference varied by model specification. Our approach provides a blueprint for combining chemical exposures linked to common adverse outcomes, and should be considered in future exposure, risk, and epidemiological studies. [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]

Scientific understanding of the etiology of uterine leiomyomata (UL) remains incomplete, but recent investigations have suggested an association between low Vitamin D and UL risk. In this study, we conducted a cross-sectional analysis of Vitamin D exposure, measured using serum levels of 25(OH)D (a Vitamin D metabolite), and self-reported UL diagnosis among 3590 women aged 20–54 in the National Health and Nutrition Examination Survey (NHANES 2001–2006). Multivariate logistic regression models comparing each quartile of 25(OH)D to the lowest quartile indicated no relationship between 25(OH)D and odds of UL in the whole population ( P trend = 0.37), or in sensitivity analyses. However, a probabilistic analysis correcting outcome misclassification indicated that insufficient 25(OH)D was associated with UL in white (Odds ratio (OR) median estimate: 2.17; 2.5, 97.5 percentiles: (1.26, 23.47)), but not black women (OR median estimate: 1.70; 2.5, 97.5 percentiles: (0.89, 3.51)), suggesting misclassification may have driven some of the null findings. [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]

Prenatal exposures to polybrominated diphenyl ethers (PBDEs) can harm neurodevelopment in humans and animals. In 2003- 2004, PentaBDE and OctaBDE were banned in California and phased-out of US production; resulting impacts on human exposures are unknown. We previously reported that median serum concentrations of PBDEs and their metabolites (OH-PBDEs) among second trimester pregnant women recruited from San Francisco General Hospital (2008-2009; n = 25) were the highest among pregnant women worldwide. We recruited another cohort from the same clinic in 2011-2012 (n = 36) and now compare serum concentrations of PBDEs, OH-PBDEs, polychlorinated biphenyl ethers (PCBs) (structurally similar compounds banned in 1979), and OHPCBs between two demographically similar cohorts. Between 2008-2009 and 2011-2012, adjusted least-squares geometric mean (LSGM) concentrations of ΣPBDEs decreased 65% (95% CI: 18, 130) from 90.0 ng/g lipid (95% CI: 64.7, 125.2) to 54.6 ng/g lipid (95% CI: 39.2, 76.2) (p = 0.004); ΣOH-PBDEs decreased 6-fold (p < 0.0001); and BDE-47, -99, and -100 declined more than BDE-153. There was a modest, nonsignificant (p = 0.13) decline in LSGM concentrations of ΣPCBs and minimal differences in ΣOH-PCBs between 2008-2009 and 2011-2012. PBDE exposures are likely declining due to regulatory action, but the relative stability in PCB exposures suggests PBDE exposures may eventually plateau and persist for decades. [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]

Prenatal exposure to polybrominated diphenyl ethers (PBDEs) may disrupt thyroid function and contribute to adverse neurodevelopmental outcomes. We conducted a pilot study to explore the relationship between serum concentrations of lower-brominated PBDEs (BDE-17 to -154), higher-brominated PBDEs (BDE-183 to -209), and hydroxylated PBDE metabolites (OH-PBDEs) with measures of thyroid function in pregnant women. Concentrations of PBDEs, OH-PBDEs, thyroid-stimulating hormone (TSH), total thyroxine (T4), and free T4 were measured in serum samples collected between 2008 and 2009 from 25 second trimester pregnant women in California. Median concentrations of lower-brominated PBDEs and OH-PBDEs were the highest reported to date in pregnant women. Median concentrations of BDE-47 and the sum of lower-brominated PBDEs (ΣPBDE5) were 43.1 ng/g lipid and 85.8 ng/g lipid, respectively, and the sum of OH-PBDEs (ΣOH-PBDE4) was 0.084 ng/mL. We observed a positive association between the weighted sum of chemicals known to bind to transthyretin (ΣTTR binders) and TSH levels. We also found positive associations between TSH and ΣPBDE5, ΣOH-PBDE4, BDE-47, BDE-85, 5-OH-BDE47, and 4'-OH-BDE49, and an inverse association with BDE-207. Relationships with free and total T4 were weak and inconsistent. Our results indicate that PBDE exposures are elevated in pregnant women in California and suggest a relationship with thyroid function. Further investigation is warranted to characterize the risks of PBDE exposures during pregnancy. [ABSTRACT FROM AUTHOR]

Children living near hazardous waste sites may be exposed to environmental contaminants, yet few studies have conducted multi-media exposure assessments, including residential environments where children spend most of their time. We sampled yard soil, house dust, and particulate matter with aerodynamic diameter <2.5 in 59 homes of young children near an abandoned mining area and analyzed samples for lead (Pb), zinc (Zn), cadmium (Cd), arsenic (As), and manganese (Mn). In over half of the homes, dust concentrations of Pb, Zn, Cd, and As were higher than those in soil. Proximity to mine waste (chat) piles and the presence of chat in the driveway significantly predicted dust metals levels. Homes with both chat sources had Pb, Zn, Cd, and As dust levels two to three times higher than homes with no known chat sources after controlling for other sources. In contrast, Mn concentrations in dust were consistently lower than in soil and were not associated with chat sources. Mn dust concentrations were predicted by soil concentrations and occupant density. These findings suggest that nearby outdoor sources of metal contaminants from mine waste may migrate indoors. Populations farther away from the mining site may also be exposed if secondary uses of chat are in close proximity to the home. [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]

Background: Household cleaning and pesticide products may contribute to breast cancer because many contain endocrine disrupting chemicals or mammary gland carcinogens. This population-based case-control study investigated whether use of household cleaners and pesticides increases breast cancer risk. Methods: Participants were 787 Cape Cod, Massachusetts, women diagnosed with breast cancer between 1988 and 1995 and 721 controls. Telephone interviews asked about product use, beliefs about breast cancer etiology, and established and suspected breast cancer risk factors. To evaluate potential recall bias, we stratified product-use odds ratios by beliefs about whether chemicals and pollutants contribute to breast cancer; we compared these results with odds ratios for family history (which are less subject to recall bias) stratified by beliefs about heredity. Results: Breast cancer risk increased two-fold in the highest compared with lowest quartile of self-reported combined cleaning product use (Adjusted OR = 2.1, 95% CI: 1.4, 3.3) and combined air freshener use (Adjusted OR = 1.9, 95% CI: 1.2, 3.0). Little association was observed with pesticide use. In stratified analyses, cleaning products odds ratios were more elevated among participants who believed pollutants contribute "a lot" to breast cancer and moved towards the null among the other participants. In comparison, the odds ratio for breast cancer and family history was markedly higher among women who believed that heredity contributes "a lot" (OR = 2.6, 95% CI: 1.9, 3.6) and not elevated among others (OR = 0.7, 95% CI: 0.5, 1.1). Conclusions: Results of this study suggest that cleaning product use contributes to increased breast cancer risk. However, results also highlight the difficulty of distinguishing in retrospective self-report studies between valid associations and the influence of recall bias. Recall bias may influence higher odds ratios for product use among participants who believed that chemicals and pollutants contribute to breast cancer. Alternatively, the influence of experience on beliefs is another explanation, illustrated by the protective odds ratio for family history among women who do not believe heredity contributes "a lot." Because exposure to chemicals from household cleaning products is a biologically plausible cause of breast cancer and avoidable, associations reported here should be further examined prospectively. [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]

Background: Accumulating evidence has shown an increased risk of type 2 diabetes in general populations exposed to arsenic, but little is known about exposures during pregnancy and the association with gestational diabetes (GD). Objectives: We studied 532 women living proximate to the Tar Creek Superfund Site to investigate whether arsenic exposure is associated with impaired glucose tolerance during pregnancy. Methods: Blood glucose was measured between 24 and 28 weeks gestation after a 1-hr oral glucose tolerance test (GTT) as part of routine prenatal care. Blood and hair were collected at delivery and analyzed for arsenic using inductively coupled plasma mass spectrometry with dynamic reaction cell. Results: Arsenic concentrations ranged from 0.2 to 24.1 μg/L (ppb) (mean ± SD, 1.7 ±1.5) and 1.1 to 724.4 ng/g (ppb) (mean ± SD, 27.4 ± 61.6) in blood and hair, respectively. One-hour glucose levels ranged from 40 to 284 mg/dL (mean ± SD, 108.7 ± 29.5); impaired glucose tolerance was observed in 11.9% of women when using standard screening criterion (> 140 mg/dL). Adjusting for age, Native-American race, prepregnancy body mass index, Medicaid use, and marital status, women in the highest quartile of blood arsenic exposure had 2.8 higher odds of impaired GTT than women in the lowest quartile of exposure (95% confidence interval, 1.1-6.9) (p-trend = 0.008). Conclusions: Among this population of pregnant women, arsenic exposure was associated with increased risk of impaired GTT at 24-28 weeks gestation and therefore may be associated with increased risk of GD. [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 (

Background: The developing kidney is vulnerable to prenatal environmental factors such as metal exposure, potentially altering the risk of later-life kidney dysfunction. This study examines the relationship between prenatal metal exposures, individually and as mixtures, and adolescent kidney function in Project Viva, a prospective longitudinal birth cohort in Massachusetts, USA. Methods: We used data on metals measured in blood during pregnancy including 15 in the first trimester and four in the second trimester. We calculated estimated glomerular filtration rate (eGFR) in adolescents (mean: 17.7 years) using cystatin C- (eGFRcys) and creatinine-based (eGFRcreat) equations for children. We used linear regression for single metal analyses, and Bayesian kernel machine regression and quantile-based g-computation for mixture analyses, adjusting for relevant covariates. To account for multiple comparisons in the single metal analyses, we applied the Holm-Bonferroni procedure to control the false discovery rate. Results: This study included 371 participants with first trimester metals and adolescent eGFR, and 256 with second trimester metals. Each doubling in first trimester cadmium concentration was associated with lower adolescent eGFRcys (β:-1.51; 95% CI:-2.83, -0.18). Each doubling in first trimester chromium (β:-1.45; 95% CI:-2.71, -0.19), nickel (β:-1.91; 95% CI:-3.65, -0.16), and vanadium (β:-1.69; 95% CI:-3.21, -0.17) was associated with lower adolescent eGFRcreat. After adjusting for multiple comparisons, p-values for associations between adolescent eGFR and chromium, nickel, vanadium and cadmium did not meet the criteria for significance. Metal mixture analyses did not identify statistically significant associations with adolescent eGFR. Conclusions: These findings have important implications for future studies investigating the potential mechanisms through which prenatal metal exposures affect long-term kidney health in children. [ABSTRACT FROM AUTHOR]

Uterine leiomyomas (fibroids) are the most common non-cancerous tumors affecting women. Psychosocial stress is associated with fibroid risk and severity. The relationship between psychosocial stress and fibroid pathogenesis may involve alterations in microRNAs (miRNAs) although this has yet to be examined. We investigated associations between two psychosocial stress measures, a composite measure of recent stressful life events and perceived social status, with expression levels of 401 miRNAs in myometrium (n = 20) and fibroids (n = 44; 20 with paired fibroid and myometrium samples) among pre-menopausal women who underwent surgery for fibroid treatment. We used linear regressions to identify psychosocial stressors associated with miRNAs, adjusting for covariates (age, body mass index, race/ethnicity, and oral contraceptive use). The association between psychosocial stressors and miRNAs was considered statistically significant at an FDR p < 0.10 and showed a monotonic response (nominal p-trend < 0.05). In the myometrium, 21 miRNAs were significantly associated with a composite measure of recent stressful events, and two miRNAs were associated with perceived social status. No fibroid miRNAs were associated with either stress measure. Pathway analyses revealed miRNA-mRNA targets were significantly enriched (FDR p < 0.05) in pathways relevant to cancer/tumor development. Of the 74 differentially expressed miRNAs between myometrium and fibroids, miR-27a-5p and miR-301b were also associated with stress exposure. Our pilot analysis suggests that psychosocial stress is associated with myometrial miRNA expression and, thus, may have a role in the pathogenesis of fibroids from healthy myometrium. [ABSTRACT FROM AUTHOR]

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]

In this article the authors discusses whether or not polybrominated diphenyl ethers (PBDEs) are a concern for environmental equity and how socioeconomic status impacts the disparities of exposure to PBDEs. Topics include an overview of several exposure assessment studies documenting the burden levels of PBDEs across various populations, racial and ethnic differences in PBDE exposure, and potential causes for disproportionate exposures, such as furniture quality.

A response by Ami R. Zota, Ruthann A. Rudel, Rachel A. Morello-Frosch, and Julia Green Brody is presented to a letter to the editor about their article "Elevated House Dust and Serum Concentrations of PBDEs in California: Unintended Consequences of Furniture Flammability Standards?” in an issue of 2008.

The article provides an update on the Project Viva study. The study was a pre-birth cohort that began in 1999-2002 in Massachusetts and aimed to examine the long-term health outcomes of women and their offspring. The study collected data on various aspects of women's health, behavior, and environment through questionnaires, in-person measurements, blood tests, and genetic analysis. The study produced numerous publications and was recently focused on analyzing data from the Mid-Life Visit, Year 19 questionnaire, and annual survey. The study's strengths include the collection of exposure and outcome measures using research standard procedures, but limitations include loss to follow-up and limited generalizability. [Extracted from the article]

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]

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]

Background: Leukocyte telomere length (LTL) is a biomarker of the aging process and is associated with the risk of chronic disease. Higher exposure to cadmium may be associated with shorter LTL, and adequate nutrient concentrations may be associated with longer LTL; however, the potential interaction between metals and nutrients on LTL has yet to be examined.Objectives: The objective of this study was to evaluate whether serum concentrations of vitamins and carotenoids were associated with LTL, and whether they modified the association between blood cadmium and LTL in the US NHANES (1999-2002).Methods: We evaluated cross-sectional associations between LTL and serum concentrations of vitamin A, γ-tocopherol, α-tocopherol, folate, and vitamin B-12 (1999-2002; n = 7458) and α-carotene, β-carotene, β-cryptoxanthin, lutein + zeaxanthin, and lycopene (2001-2002; n = 4018) in a nationally representative sample of US adults (≥20 y of age) with the use of multivariable linear regression. We further investigated whether vitamin and carotenoid concentrations modified associations between blood cadmium and LTL with models stratified by serum nutrient concentrations and the inclusion of an interaction term.Results: Blood cadmium was inversely associated with LTL (percentage of LTL difference per 1 μg/L = -3.74; 95% CI: -5.35, -2.10). Serum vitamin A was positively associated (percentage of LTL difference per 1 μg/L = 4.01; 95% CI: 0.26, 7.90) and γ-tocopherol was inversely associated (percentage of LTL difference per 1 μg/dL = -2.49; 95% CI: -4.21, -0.73) with LTL. Serum folate (P-trend = 0.06) and α-tocopherol (P-trend = 0.10) were marginally positively associated with LTL, whereas vitamin B-12 (P-trend = 0.78) was not associated with LTL. Serum carotenoids were generally positively associated with LTL. Serum vitamin and carotenoid concentrations did not modify blood cadmium and LTL associations (P-interaction > 0.10).Conclusions: Results from this cross-sectional study suggest that exposure to cadmium and certain nutrients may be associated with LTL in US adults, but the serum concentrations of the vitamins and carotenoids evaluated did not modify cross-sectional associations between cadmium exposure and LTL. [ABSTRACT FROM AUTHOR]

Racial/ethnic disparities in hypertension are a pressing public health problem. The contribution of environmental pollutants including PFAS have not been explored, even though certain PFAS are higher in Black population and have been associated with hypertension. We examined the extent to which racial/ethnic disparities in incident hypertension are explained by racial/ethnic differences in serum PFAS concentrations. We included 1058 hypertension-free midlife women with serum PFAS concentrations in 1999–2000 from the multi-racial/ethnic Study of Women's Health Across the Nation with approximately annual follow-up visits through 2017. Causal mediation analysis was conducted using accelerated failure time models. Quantile-based g-computation was used to evaluate the joint effects of PFAS mixtures. During 11,722 person-years of follow-up, 470 participants developed incident hypertension (40.1 cases per 1000 person-years). Black participants had higher risks of developing hypertension (relative survival: 0.58, 95% CI: 0.45–0.76) compared with White participants, which suggests racial/ethnic disparities in the timing of hypertension onset. The percent of this difference in timing that was mediated by PFAS was 8.2% (95% CI: 0.7–15.3) for PFOS, 6.9% (95% CI: 0.2–13.8) for EtFOSAA, 12.7% (95% CI: 1.4–22.6) for MeFOSAA, and 19.1% (95% CI: 4.2, 29.0) for PFAS mixtures. The percentage of the disparities in hypertension between Black versus White women that could have been eliminated if everyone's PFAS concentrations were dropped to the 10th percentiles observed in this population was 10.2% (95% CI: 0.9–18.6) for PFOS, 7.5% (95% CI: 0.2–14.9) for EtFOSAA, and 17.5% (95% CI: 2.1–29.8) for MeFOSAA. These findings suggest differences in PFAS exposure may be an unrecognized modifiable risk factor that partially accounts for racial/ethnic disparities in timing of hypertension onset among midlife women. The study calls for public policies aimed at reducing PFAS exposures that could contribute to reductions in racial/ethnic disparities in hypertension. • PFAS exposure may account for racial/ethnic disparities in hypertension incidence. • Certain PFAS could explain 7–10% of the Black-White disparities in hypertension. • PFAS mixtures could explain 19.1% of the Black-White disparities in hypertension. [ABSTRACT FROM AUTHOR]

Background: Bisphenol A (BPA) is a ubiquitous, endocrine-disrupting environmental contaminant that increases risk of some adverse developmental effects. Thus, it is important to characterize BPA levels, metabolic fate and sources of exposure in pregnant women.Methods: We used an improved liquid chromatography-tandem mass spectrometry (LC-MS/MS) analytic method to directly and simultaneously measure unconjugated BPA (uBPA), BPA glucuronide and BPA sulfate in the urine of a population of ethnically and racially diverse, and predominately low-income pregnant women (n = 112) in their second trimester. We also administered a questionnaire on dietary and non-dietary sources of exposure to BPA.Results: We found universal and high exposure to uBPA and its metabolites: median concentrations were 0.25, 4.67, and 0.31 μg/g creatinine for uBPA, BPA glucuronide, and BPA sulfate, respectively. The median Total BPA (uBPA + BPA in glucuronide and sulfate forms) level was more than twice that measured in U.S. pregnant women in NHANES 2005-2006, while 30 % of the women had Total BPA levels above the 95th percentile. On average, Total BPA consisted of 71 % BPA in glucuronide form, 15 % BPA in sulfate form and 14 % uBPA, however the proportion of BPA in sulfate form increased and the proportion of uBPA decreased with Total BPA levels. Occupational and non-occupational contact with paper receipts was positively associated with BPA in conjugated (glucuronidated + sulfated) form after adjustment for demographic characteristics. Recent consumption of foods and beverages likely to be contaminated with BPA was infrequent among participants and we did not observe any positive associations with BPA analyte levels.Conclusion: The high levels of BPA analytes found in our study population may be attributable to the low-income status of the majority of participants and/or our direct analytic method, which yields a more complete evaluation of BPA exposure. We observed near-universal exposure to BPA among pregnant women, as well as substantial variability in BPA metabolic clearance, raising additional concerns for effects on fetal development. Our results are consistent with studies showing thermal paper receipts to be an important source of exposure, point to the difficulty pregnant women have avoiding BPA exposure on an individual level, and therefore underscore the need for changes in BPA regulation and commerce. [ABSTRACT FROM AUTHOR]

Background: Substandard housing conditions and hazardous indoor environmental exposures contribute to significant morbidity and mortality worldwide. Housing indices that capture the multiple dimensions of healthy housing are important for tracking conditions and identifying vulnerable households. However, most indices focus on physical deficiencies and repair costs and omit indoor environmental exposures, as few national data sources routinely collect this information. Methods: We developed a multidimensional Housing and Environmental Quality Index (HEQI) based on the World Health Organization's Housing and Health Guidelines and applied it to the 2019 American Housing Survey (AHS). The HEQI consisted of ten domains associated with poor health: household fuel combustion, dampness and mold, pests and allergens, lead paint risk, high indoor temperatures, low indoor temperatures, household crowding, injury hazards, inadequate water and sanitation, and ventilation. We evaluated the validity and performance of the HEQI against three housing characteristics (i.e., year built, monthly rent costs, unit satisfaction rating) and two established indices (i.e., Adequacy Index, Poor Quality Index). Results: Approximately 79% (92 million) of U.S. households reported at least one HEQI domain associated with poor health (mean per household: 1.3; range: 0,8). Prevalent domains included household fuel combustion (61.4%), dampness and mold (15.9%), inadequate water and sanitation (14.3%), and injury hazards (11.9%). Pests and allergens, low indoor temperatures, and injury hazards were consistently associated with older homes, lower rent costs, and lower unit satisfaction. Compared to established housing indices, the HEQI captured four new environmental domains which enabled the identification of 57.7 million (63%) more households with environmental risk factors like mold, cockroaches, crowding, household fuel combustion, and higher building leakage. Conclusions: Indoor environmental exposures are prevalent in U.S. households and not well-captured by existing housing indices. The HEQI is a multidimensional tool that can be used to monitor indoor environmental exposures and housing quality trends in the U.S. Some domains, including radon, pesticides, asbestos, noise, and housing accessibility could not be assessed due to the lack of available data in the AHS. The mounting evidence linking residential environmental exposures with adverse health outcomes underscore the need for this data in the AHS and other national surveys. [ABSTRACT FROM AUTHOR]

Background: Substandard housing conditions and hazardous indoor environmental exposures contribute to significant morbidity and mortality worldwide. Housing indices that capture the multiple dimensions of healthy housing are important for tracking conditions and identifying vulnerable households. However, most indices focus on physical deficiencies and repair costs and omit indoor environmental exposures, as few national data sources routinely collect this information.Methods: We developed a multidimensional Housing and Environmental Quality Index (HEQI) based on the World Health Organization's Housing and Health Guidelines and applied it to the 2019 American Housing Survey (AHS). The HEQI consisted of ten domains associated with poor health: household fuel combustion, dampness and mold, pests and allergens, lead paint risk, high indoor temperatures, low indoor temperatures, household crowding, injury hazards, inadequate water and sanitation, and ventilation. We evaluated the validity and performance of the HEQI against three housing characteristics (i.e., year built, monthly rent costs, unit satisfaction rating) and two established indices (i.e., Adequacy Index, Poor Quality Index).Results: Approximately 79% (92 million) of U.S. households reported at least one HEQI domain associated with poor health (mean per household: 1.3; range: 0,8). Prevalent domains included household fuel combustion (61.4%), dampness and mold (15.9%), inadequate water and sanitation (14.3%), and injury hazards (11.9%). Pests and allergens, low indoor temperatures, and injury hazards were consistently associated with older homes, lower rent costs, and lower unit satisfaction. Compared to established housing indices, the HEQI captured four new environmental domains which enabled the identification of 57.7 million (63%) more households with environmental risk factors like mold, cockroaches, crowding, household fuel combustion, and higher building leakage.Conclusions: Indoor environmental exposures are prevalent in U.S. households and not well-captured by existing housing indices. The HEQI is a multidimensional tool that can be used to monitor indoor environmental exposures and housing quality trends in the U.S. Some domains, including radon, pesticides, asbestos, noise, and housing accessibility could not be assessed due to the lack of available data in the AHS. The mounting evidence linking residential environmental exposures with adverse health outcomes underscore the need for this data in the AHS and other national surveys. [ABSTRACT FROM AUTHOR]

Uterine leiomyomas are the most common pelvic tumor in women of reproductive age; they cause irregular heavy menstrual bleeding leading to anemia and subsequent negative effects on quality of life. Exosomes have arisen as main players of disease progression in several illnesses, including a range of benign and malignant conditions; however, their role in leiomyomas' pathophysiology remains unknown. We investigated the effect of exosomes derived from human uterine leiomyoma tumor cells (HULM) and human myometrial cells (UTSM) on the behavior of human endometrial microvascular endothelial cells (HEMEC). HULM- and UTSM-derived exosomes were isolated and cocultured with HEMECs. Then, cell proliferation, mRNA expression, tube formation assay, and RNA-seq were performed. Treatment of HEMEC with HULM-derived exosomes increased cell proliferation by 60% compared to control untreated cells, upregulated C-MYC and VEGFA expression levels, and increased tube formation, length, and branching (markers of angiogenesis). Profiling of miRNA revealed that 84 miRNAs were significantly downregulated and 71 were upregulated in HULM-derived exosomes compared to UTSM-derived exosomes. These findings suggest that HULM-derived exosomes might have effects on HEMEC function, containing factors that enhance endometrial proliferation and angiogenesis, which may contribute to heavy menstrual bleeding. Further research on exosomes in uterine leiomyoma may identify possible novel biomarkers for treatment. [ABSTRACT FROM AUTHOR]

An editorial is presented in which the authors discuss the intersection of racism, sexism, and classism with what is termed the environmental injustice of beauty products and the beauty products industry. It examines the health impact of unequal chemical problems for Black and Latina women, regulation of the cosmetics industry by the U.S. government, and the concept of clean beauty.

[Display omitted] • PFOS was associated with higher parameters of gestational BP trajectories. • Positive associations were stronger in participants with parity ≥ 1. Evidence suggests that exposure to per- and polyfluoroalkyl substances (PFAS) increases risk of high blood pressure (BP) during pregnancy. Prior studies did not examine associations with BP trajectory parameters (i.e., overall magnitude and velocity) during pregnancy, which is linked to adverse pregnancy outcomes. To estimate associations of multiple plasma PFAS in early pregnancy with BP trajectory parameters across the second and third trimesters. To assess potential effect modification by maternal age and parity. In 1297 individuals, we quantified six PFAS in plasma collected during early pregnancy (median gestational age: 9.4 weeks). We abstracted from medical records systolic BP (SBP) and diastolic BP (DBP) measurements, recorded from 12 weeks gestation until delivery. BP trajectory parameters were estimated via Super Imposition by Translation and Rotation modeling. Subsequently, Bayesian Kernel Machine Regression (BKMR) was employed to estimate individual and joint associations of PFAS concentrations with trajectory parameters – adjusting for maternal age, race/ethnicity, pre-pregnancy body mass index, income, parity, smoking status, and seafood intake. We evaluated effect modification by age at enrollment and parity. We collected a median of 13 BP measurements per participant. In BKMR, higher concentration of perfluorooctane sulfonate (PFOS) was independently associated with higher magnitude of overall SBP and DBP trajectories (i.e., upward shift of trajectories) and faster SBP trajectory velocity, holding all other PFAS at their medians. In stratified BKMR analyses, participants with ≥ 1 live birth had more pronounced positive associations between PFOS and SBP velocity, DBP magnitude, and DBP velocity – compared to nulliparous participants. We did not observe significant associations between concentrations of the overall PFAS mixture and either magnitude or velocity of the BP trajectories. Early pregnancy plasma PFOS concentrations were associated with altered BP trajectory in pregnancy, which may impact future cardiovascular health of the mother. [ABSTRACT FROM AUTHOR]

Black women are more likely to undergo surgery for uterine fibroids compared with non-Black women. However, few studies have characterized the psychosocial experiences of Black women seeking fibroid treatment. We aimed to identify factors that shape Black women's fibroid management decisions; explore how discrimination based on race, class, and gender feature in treatment-seeking experiences, and compare experiences across age and socioeconomic status. We conducted semistructured interviews with 37 Black women undergoing surgery for fibroid management. We used a thematic analysis to code transcripts and identify themes. Participants were predominately single, college educated, and insured. Respondents reported that patient–doctor interactions, support from social networks, fertility consequences, and fear of fibroid malignancy influenced their fibroid management decisions. Knowledge and perceptions of fibroids were also influenced by community norms and differed by socioeconomic status; women of higher socioeconomic status had greater fibroid awareness than women of lower socioeconomic status. Discrimination was discussed in the context of historical inequity against Black women, with one participant questioning whether Black women were valued less in clinical settings compared with non-Black women. Although several women discussed positive experiences seeking fibroids care, others expressed medical mistrust or said that alternative management options were not offered by clinicians. Fibroid management decisions were influenced not only by interactions with clinicians and social networks, and concerns about fertility and fibroid malignancy, but also by broader social and historical conditions. These findings suggest that clinicians should deliver intersectional gynecologic care that centers the voices of Black women seeking fibroid treatment. [ABSTRACT FROM AUTHOR]

Robust data from longitudinal birth cohort studies and experimental studies of perinatally exposed animals indicate that exposure to ortho-phthalates can impair brain development and increase risks for learning, attention, and behavioral disorders in childhood. This growing body of evidence, along with known adverse effects on male reproductive tract development, calls for immediate action. Exposures are ubiquitous; the majority of people are exposed to multiple ortho-phthalates simultaneously. We thus recommend that a class approach be used in assessing health impacts as has been done with other chemical classes. We propose critically needed policy reforms to eliminate ortho-phthalates from products that lead to exposure of pregnant women, women of reproductive age, infants, and children. Specific attention should be focused on reducing exposures among socially vulnerable populations such as communities of color, who frequently experience higher exposures. Ortho-phthalates are used in a vast array of products and elimination will thus necessitate a multipronged regulatory approach at federal and state levels. The fact that manufacturers and retailers have already voluntarily removed ortho-phthalates from a wide range of products indicates that this goal is feasible. [ABSTRACT FROM AUTHOR]

Highlights • Endocrine-disrupting chemicals are present in products used in the vaginal area. • Effects of endocrine-disrupting chemicals on the vaginal microbiome are unknown. • Some phthalate metabolites were bivariately associated with bacterial vaginosis. • Associations were attenuated after adjustment for urinary creatinine. • Novel methods of directly measuring intravaginal chemical exposures are needed. Abstract Endocrine-disrupting chemicals, such as phthalates, are an unexamined potential risk factor for bacterial vaginosis (BV) and warrant investigation because hormones affect BV. We examined the association between phthalate exposure and BV in the National Health and Nutrition Examination Survey, 2001–2004. BV outcomes were defined as intermediate (Nugent score of 4–6) and positive (7–10). Phthalate metabolites, including monoethyl phthalate (MEP), mono- n -butyl phthalate (MnBP), and di(2-ethylhexyl) phthalate (DEHP) metabolites, were measured in urine. Among 854 women with complete data, multinomial logistic regression revealed that concentrations of MnBP (Q4 vs. Q1 OR = 3.01, 95% CI 1.76–5.15, p-trend <0.001) and ΣDEHP metabolites (Q4 OR = 2.55, 95% CI 1.45–4.47, p-trend = 0.03) were associated with Nugent-score BV, although only MnBP was significant after adjustment for confounders. Associations were null after adjustment for urinary creatinine (MnBP Q4 OR = 1.11, 95% CI 0.63–1.96; ΣDEHP Q4 OR = 0.72, 95% CI 0.37–1.39). Future work should further examine these relationships using direct measurements of intravaginal phthalates exposures. [ABSTRACT FROM AUTHOR]

Background Anti-androgenic phthalates are reproductive toxicants that may have additive effects on male development. Diet is the primary exposure source for most phthalates, which contaminate the food supply through food contact materials and industrialized production. Objective To compare dietary sources of cumulative phthalates exposure between “food at home” (e.g. food consumed from a grocery store) and “food away from home” (e.g. food consumed from fast food/restaurants and cafeterias) in the U.S. general population. Methods We estimated cumulative phthalates exposure by calculating daily intake from metabolite concentrations in urinary spot samples for 10,253 participants (≥6 years old) using National Health and Nutrition Examination Survey (NHANES, 2005–2014) data. We constructed a biologically relevant metric of phthalates daily intake (∑androgen-disruptor, μg/kg/day) by converting phthalates into anti-androgen equivalent terms prior to their summation. Particular foods and the percent of total energy intake (TEI) consumed from multiple dining out sources were ascertained from 24-h recall surveys. Associations with ∑androgen-disruptor levels were estimated for children, adolescents, and adults using multivariable linear regression. Results We observed a consistent positive association between dining out and Σandrogen-disruptor levels across the study population ( p -trend <0.0001). Among adolescents, high consumers of foods outside the home had 55% (95% CI: 35%, 78%) higher Σandrogen-disruptor levels compared to those who only consumed food at home. The contribution of specific dining out sources to Σandrogen-disruptor levels varied by age group. For example, cafeteria food was associated with 15% (95% CI: 4.0%, 28%) and 64% (95% CI: 40%, 92%) higher Σandrogen-disruptor levels in children and adults, respectively. Particular foods, especially sandwiches (i.e. cheeseburgers), were associated with increased Σandrogen-disruptor levels only if they were purchased away from home ( p  < 0.01). Conclusion Dining out may be an important source of biologically relevant cumulative phthalates exposure among the U.S. population. Future studies should evaluate modifiable production practices that remove phthalates from the food supply in addition to the efficacy of interventions that promote eating fresh foods prepared at home. [ABSTRACT FROM AUTHOR]

Some trace elements are established nephrotoxicants, yet their associations with kidney function remain understudied in the context of pregnancy, a time of substantial change in kidney physiology and function. We aimed to estimate the individual and joint associations of trace element mixtures with maternal kidney function during the 1st trimester of pregnancy (mean 9.7 gestational weeks). 1040 women from Project Viva contributed blood samples which were assessed for erythrocyte non-essential [arsenic (As), cadmium (Cd), cesium (Cs), mercury (Hg), lead (Pb)] and essential [barium (Ba), magnesium (Mg), manganese (Mn), selenium (Se), and Zinc (Zn)] trace elements, and plasma creatinine for kidney function. We estimated glomerular filtration rate using the Chronic Kidney Disease Epidemiology Collaboration (eGFR CKD-EPI) equation without race-adjustment factors. We examined associations of eGFR CKD-EPI with individual trace elements using multivariable linear regression and their mixtures using quantile-based g-computation, adjusting for sociodemographics, pregnancy characteristics, and diet. Participants in our study were predominantly White (75%), college graduates (72%), and had household income >$70,000/year (63%). After adjusting for covariates, higher Pb (β −3.51 ml/min/1.73 m2; 95% CI -5.83, −1.18) concentrations were associated with lower eGFR CKD-EPI , while higher Mg (β 10.53 ml/min/1.73 m2; 95% CI 5.35, 15.71), Se (β 5.56 ml/min/1.73 m2; 95% CI 0.82, 10.31), and Zn (β 5.88 ml/min/1.73 m2; 95% CI 0.51, 11.26) concentrations were associated with higher eGFR CKD-EPI. In mixture analyses, higher non-essential trace elements mixture concentration was associated with reduced eGFR CKD-EPI (Ψ −1.03 ml/min/1.73 m2; 95% CI: 1.92, −0.14). Conversely, higher essential trace elements mixture concentration was associated with higher eGFR (Ψ 1.42; 95% CI: 0.48, 2.37). Exposure to trace elements in early pregnancy may influence women's kidney function although reverse causation cannot be eliminated in this cross-sectional analysis. These findings have important implications for long-term cardiovascular and postpartum kidney health that warrant additional studies. • Cross-sectional study of blood trace elements and kidney function in 1st trimester. • A higher level of lead was associated with lower eGFR. • Higher levels of magnesium, selenium, and zinc were associated with higher eGFR. • Non-essential trace elements mixture was associated with lower eGFR. • Essential trace elements mixture was associated with higher eGFR. [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]

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]

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]

Background: Diethyl phthalate (DEP) and di-n-butyl phthalate (DnBP) are industrial chemicals found in consumer products that may increase risk of adverse health effects. Although use of personal care/beauty products is known to contribute to phthalate exposure, no prior study has examined feminine hygiene products as a potential phthalate source. In this study, we evaluate whether vaginal douching and other feminine hygiene products increase exposure to phthalates among US reproductive-aged women. Methods: We conducted a cross-sectional study on 739 women (aged 20-49) from the National Health and Nutrition Examination Survey 2001-2004 to examine the association between self-reported use of feminine hygiene products (tampons, sanitary napkins, vaginal douches, feminine spray, feminine powder, and feminine wipes/towelettes) with urinary concentrations of monoethyl phthalate (MEP) and mono-n-butyl phthalate (MnBP), metabolites of DEP and DnBP, respectively. Results: A greater proportion of black women than white and Mexican American women reported use of vaginal douches, feminine spray, feminine powder, and wipes/towelettes in the past month whereas white women were more likely than other racial/ethnic groups to report use of tampons (p < 0.05). Douching in the past month was associated with higher concentrations of MEP but not MnBP. No other feminine hygiene product was significantly associated with either MEP or MnBP. We observed a dose-response relationship between douching frequency and MEP concentrations (ptrend < 0.0001); frequent users (=2 times/month) had 152.2 % (95 % confidence intervals (CI): (68.2 %, 278.3 %)) higher MEP concentrations than non-users. We also examined whether vaginal douching mediates the relationship between race/ethnicity and phthalates exposures. Black women had 48.4 % (95 % CI: 16.8 %, 88.6 %; p = 0.0002) higher MEP levels than white women. Adjustment for douching attenuated this difference to 26.4 % (95 % CI:-0.9 %, 61.2 %; p = 0.06). Mediation effects of douching were statistically significant for black-white differences (z = 3.71, p < 0.001) but not for differences between Mexican Americans and whites (z = 1.80, p = 0.07). Conclusions: Vaginal douching may increase exposure to DEP and contribute to racial/ethnic disparities in DEP exposure. The presence of environmental chemicals in vaginal douches warrants further examination. [ABSTRACT FROM AUTHOR]

Background: Diethyl phthalate (DEP) and di-n-butyl phthalate (DnBP) are industrial chemicals found in consumer products that may increase risk of adverse health effects. Although use of personal care/beauty products is known to contribute to phthalate exposure, no prior study has examined feminine hygiene products as a potential phthalate source. In this study, we evaluate whether vaginal douching and other feminine hygiene products increase exposure to phthalates among US reproductive-aged women. Methods: We conducted a cross-sectional study on 739 women (aged 20–49) from the National Health and Nutrition Examination Survey 2001–2004 to examine the association between self-reported use of feminine hygiene products (tampons, sanitary napkins, vaginal douches, feminine spray, feminine powder, and feminine wipes/towelettes) with urinary concentrations of monoethyl phthalate (MEP) and mono-n-butyl phthalate (MnBP), metabolites of DEP and DnBP, respectively. Results: A greater proportion of black women than white and Mexican American women reported use of vaginal douches, feminine spray, feminine powder, and wipes/towelettes in the past month whereas white women were more likely than other racial/ethnic groups to report use of tampons (p < 0.05). Douching in the past month was associated with higher concentrations of MEP but not MnBP. No other feminine hygiene product was significantly associated with either MEP or MnBP. We observed a dose–response relationship between douching frequency and MEP concentrations (ptrend < 0.0001); frequent users (≥2 times/month) had 152.2 % (95 % confidence intervals (CI): (68.2 %, 278.3 %)) higher MEP concentrations than non-users. We also examined whether vaginal douching mediates the relationship between race/ethnicity and phthalates exposures. Black women had 48.4 % (95 % CI: 16.8 %, 88.6 %; p = 0.0002) higher MEP levels than white women. Adjustment for douching attenuated this difference to 26.4 % (95 % CI:−0.9 %, 61.2 %; p = 0.06). Mediation effects of douching were statistically significant for black-white differences (z = 3.71, p < 0.001) but not for differences between Mexican Americans and whites (z = 1.80, p = 0.07). Conclusions: Vaginal douching may increase exposure to DEP and contribute to racial/ethnic disparities in DEP exposure. The presence of environmental chemicals in vaginal douches warrants further examination. [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]