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There are known health concerns linked to prenatal tobacco and cannabis exposures. This study aims to objectively determine the level of exposure to tobacco and cannabis in pregnant individuals from six race/ethnicity groups (Black, Hispanic, Asian Indian, Native American, Vietnamese, and White) in the first three years following legalization of recreational marijuana use in 2018 in California. We used a cross-sectional sample of prenatal screening program participants (2018-2020) from southern and central California (N = 925). Exposures were estimated by a lab analysis of cotinine (tobacco) and 11-hydroxy-Δ9-tetrahydrocannabinol (OH-THC, cannabis) in banked serum. Disparities in tobacco exposure were evident, with Black subjects experiencing the highest smoking rate (16%) followed by Native American (10%) and White (8%) subjects, and ≤2% among Hispanic, Asian Indian, and Vietnamese subjects. Environmental tobacco exposure generally showed a similar pattern of exposure to tobacco smoking across race/ethnicity groups. Cannabis detection ranged from 5% among Hispanic subjects to 12% and 13% among White and Black subjects, respectively, and was higher among tobacco users and those exposed to environmental tobacco smoke than those with no cotinine detected. Tobacco and cannabis exposure were generally greatest in younger subjects and those with indices of a lower economic status; however, among Black subjects, cannabis exposure was greatest in older subjects and those with a higher socioeconomic status. Race/ethnicity, age, and socioeconomic factors can inform targeting of high-exposure groups for intervention.

Immune dysregulation, including aberrant peripheral cytokine/chemokine levels, is implicated in neurodevelopmental disorders (NDD) such as autism spectrum disorder (ASD). While the diagnosis of ASD is more common in males compared to females, sex effects in immune dysregulation related to neurodevelopment remain understudied. The aim of this exploratory study was to determine whether there are sex-specific effects in neonatal immune dysregulation with respect to an ASD or delayed development (DD) diagnosis. We utilized the data from the Early Markers for Autism study, a population based case-control study of prenatal and neonatal biomarkers of ASD. The immune profile of newborns later diagnosed with ASD (n = 482, 91 females), DD (n = 140, 61 females) and sex-matched general population controls (GP; n = 378, 67 females) were analyzed using neonatal bloodspots (NBS) via 42-plex multiplex assay. Multiple linear regression analysis was performed to identify whether sex was associated with differences in cytokine/chemokine levels of children with ASD, DD, and GP. A sex by diagnosis interaction effect was observed only for the chemokine macrophage migration inhibitory factor (MIF), with males displaying higher levels of NBS MIF than females in the GP control group (p = 0.02), but not in ASD (p = 0.52) or DD (p = 0.29) groups. We found that regardless of child diagnosis, newborn bloodspot eluates from females had a significantly higher concentration than males with the same diagnosis of the chemokines granulocyte chemotactic protein 2 (GCP-2; p

Exposures to phthalates, parabens, and other phenols are often correlated due to their ubiquitous use in personal care products and plastics. Examining these compounds as a complex mixture may clarify inconsistent relationships between individual chemicals and childhood adiposity. Using data from the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS) study, a longitudinal cohort of children in Salinas Valley, California (n = 309), we examined biomarkers of 11 phthalate metabolites and 9 phenols, including several parabens and bisphenol A, measured in maternal urine at two time points during pregnancy. We measured child height and weight at age five to calculate the body mass index (BMI) z-scores and overweight/obesity status. The association between prenatal urinary concentrations of biomarkers with the childhood BMI z-score and overweight/obesity status was analyzed using single-pollutant models and two mixture methods: Bayesian hierarchical modeling (BMH) and Bayesian kernel machine regression (BKMR). Urinary concentrations of monoethyl phthalate, monocarboxy-isononly phthalate (metabolites of diethyl phthalate and di-isodecyl phthalate, respectively), and propylparaben were consistently associated with an increased BMI z-score and overweight/obesity status across all modeling approaches. Higher prenatal exposures to the cumulative biomarker mixture also trended with greater childhood adiposity. These results, robust across two methods that control for co-pollutant confounding, suggest that prenatal exposure to certain phthalates and parabens may increase the risk for obesity in early childhood.

BackgroundChemicals found in personal care products and plastics have been associated with asthma, allergies, and lung function, but methods to address real life exposure to mixtures of these chemicals have not been applied to these associations.MethodsWe quantified urinary concentrations of eleven phthalate metabolites, four parabens, and five other phenols in mothers twice during pregnancy and assessed probable asthma, aeroallergies, and lung function in their age seven children. We implemented Bayesian Profile Regression (BPR) to cluster women by their exposures to these chemicals and tested the clusters for differences in outcome measurements. We used Bayesian Kernel Machine Regression (BKMR) to fit biomarkers into one model as joint independent variables.ResultsBPR clustered women into seven groups characterized by patterns of personal care product and plastic use, though there were no significant differences in outcomes across clusters. BKMR showed that monocarboxyisooctyl phthalate and 2,4-dichlorophenol were associated with probable asthma (predicted probability of probable asthma per IQR of biomarker z-score (standard deviation) = 0.08 (0.09) and 0.11 (0.12), respectively) and poorer lung function (predicted probability per IQR = -0.07 (0.05) and -0.07 (0.06), respectively), and that mono(3-carboxypropyl) phthalate and bisphenol A were associated with aeroallergies (predicted probability per IQR = 0.13 (0.09) and 0.11 (0.08), respectively). Several biomarkers demonstrated positive additive effects on other associations.ConclusionsBPR and BKMR are useful tools to evaluate associations of biomarker concentrations within a mixture of exposure and should supplement single-chemical regression models when data allow.

Respiratory rate (RR) is a predictor of adverse outcomes. However, RRs are inaccurately measured in the hospital. We conducted a quality improvement (QI) initiative using plan-do-study-act methodology on one inpatient unit of a safety-net hospital to improve RR accuracy. We added time-keeping devices to vital sign carts and retrained patient-care assistants on a newly modified workflow that included concomitant RR measurement during automated blood pressure measurement. The median RR was 18 (interquartile range [IQR] 18-20) preintervention versus 14 (IQR 15-20) postintervention. RR accuracy, defined as ±2 breaths of gold-standard measurements, increased from 36% preintervention to 58% postintervention (P < .01). The median time for vital signs decreased from 2:36 minutes (IQR, 2:04-3:20) to 1:55 minutes (IQR, 1:40-2:22; P < .01). The intervention was associated with a 7.8% reduced incidence of tachypnea-specific systemic inflammatory response syndrome (SIRS = 2 points with RR > 20; 95% CI, -13.5% to -2.2%). Our interdisciplinary, low-cost, low-tech QI initiative improved the accuracy and efficiency of RR measurement.

BackgroundThe prevalence of asthma and allergy is increasing in US children. In utero exposure to chemicals used in personal care products and plastics may contribute to increase in these diseases.MethodsWe quantified urinary concentrations of eight phthalate metabolites and bisphenol A in mothers twice during pregnancy in 1999-2000 in Salinas, California. We assessed probable asthma, aeroallergies, eczema, and spirometry in their children at age 7, and measured T helper 1 and T helper 2 cells in blood at ages 2, 5, and 7 (N = 392). We employed Bayesian model averaging to select confounders from additional biomarkers measured in this population and controlled for them in logistic and linear regressions.ResultsMonocarboxyisooctyl phthalate was associated with increased odds for probable asthma (odds ratio: 1.54, 95% CI: 1.12, 2.12), and with lower forced expiratory volume in one second (β: -0.09 L, 95% CI: -0.15, -0.03) and forced expiratory flow from 25% to 75% of forced vital capacity (β: -7.06 L/s, 95% CI: -11.04, -2.90). Several other associations were attenuated in final models that controlled for additional biomarkers.ConclusionMonocarboxyisooctyl phthalate was associated with lower respiratory health after controlling for related chemical exposure, which suggests that confounding by multiple chemical exposures should be considered in future research.

Use of personal care products, such as makeup, soaps, and sunscreen, may expose adolescent girls to potential endocrine disruptors, including phthalates, parabens, and other phenols. We evaluated the relationship between recent self-reported personal care product use and concentrations for urinary metabolites of phthalates, parabens, triclosan, and benzophenone-3 (BP-3) in 100 Latina adolescents. Girls who reported using makeup every day vs. rarely/never had higher urinary concentrations of monoethyl phthalate (MEP) (102.2 ng/mL vs. 52.4 ng/mL, P-value: 0.04), methyl paraben (MP) (120.5 ng/mL vs. 13.4 ng/mL, P-value

Study questionAre in-utero or peripubertal exposures to phthalates, parabens and other phenols found in personal care products associated with timing of pubertal onset in boys and girls?Summary answerWe found some associations of altered pubertal timing in girls, but little evidence in boys.What is known alreadyCertain chemicals in personal care and consumer products, including low molecular weight phthalates, parabens and phenols, or their precursors, are associated with altered pubertal timing in animal studies.Study design, size, durationData were from the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS) longitudinal cohort study which followed 338 children in the Salinas Valley, California, from before birth to adolescence.Participants/materials, setting, methodsPregnant women were enrolled in 1999-2000. Mothers were mostly Latina, living below the federal poverty threshold and without a high school diploma. We measured concentrations of three phthalate metabolites (monoethyl phthalate [MEP], mono-n-butyl phthalate and mono-isobutyl phthalate), methyl and propyl paraben and four other phenols (triclosan, benzophenone-3 and 2,4- and 2,5-dichlorophenol) in urine collected from mothers during pregnancy and from children at age 9. Pubertal timing was assessed among 179 girls and 159 boys every 9 months between ages 9 and 13 using clinical Tanner staging. Accelerated failure time models were used to obtain mean shifts of pubertal timing associated with concentrations of prenatal and peripubertal biomarkers.Main results and the role of chanceIn girls, we observed earlier onset of pubic hair development with prenatal urinary MEP concentrations and earlier menarche with prenatal triclosan and 2,4-dichlorophenol concentrations. Regarding peripubertal biomarkers, we observed: earlier breast development, pubic hair development and menarche with methyl paraben; earlier menarche with propyl paraben; and later pubic hair development with 2,5-dichlorophenol. In boys, we observed no associations with prenatal urinary biomarker concentrations and only one association with peripubertal concentrations: earlier genital development with propyl paraben.Limitations, reasons for cautionThese chemicals are quickly metabolized and one to two urinary measurements per developmental point may not accurately reflect usual exposure. Associations of peripubertal measurements with parabens may reflect reverse causality: children going through puberty early may be more likely to use personal care products. The study population was limited to Latino children of low socioeconomic status living in a farmworker community and may not be widely generalizable.Wider implications of the findingsThis study contributes to a growing literature that suggests that exposure to certain endocrine disrupting chemicals may impact timing of puberty in children.Study funding/competing interest(s)This study was funded by the National Institute of Environmental Health Sciences and the US Environmental Protection Agency. The authors declare no conflicts of interest.Trial registration numberN/A.

BackgroundPersonal care product chemicals may be contributing to risk for asthma and other atopic illnesses. The existing literature is conflicting, and many studies do not control for multiple chemical exposures.MethodsWe quantified concentrations of three phthalate metabolites, three parabens, and four other phenols in urine collected twice during pregnancy from 392 women. We measured T helper 1 (Th1) and T helper 2 (Th2) cells in their children's blood at ages two, five, and seven, and assessed probable asthma, aeroallergies, eczema, and lung function at age seven. We conducted linear and logistic regressions, controlling for additional biomarkers measured in this population as selected by Bayesian Model Averaging.ResultsThe majority of comparisons showed null associations. Mono-n-butyl phthalate (MnBP) was associated with higher Th2% (RR: 10.40, 95% CI: 3.37, 17.92), and methyl paraben was associated with lower Th1% (RR: -3.35, 95% CI: -6.58, -0.02) and Th2% at borderline significance (RR: -4.45, 95% CI: -8.77, 0.08). Monoethyl phthalate was associated with lower forced expiratory flow from 25 to 75% of forced vital capacity (FEF25-75%) (RR: -3.22 L/s, 95% CI: -6.02, -0.34). Propyl paraben (OR: 0.86, 95% CI: 0.74, 0.99) was associated with decreased odds of probable asthma.ConclusionsWhile some biomarkers, particularly those from low molecular weight phthalates, were associated with an atopic cytokine profile and poorer lung function, no biomarkers were associated with a corresponding increase in atopic disease.

BackgroundAnimal studies suggest that phthalates and bisphenol A (BPA), endocrine-disrupting chemicals found in many consumer products, may impact the timing of puberty.ObjectivesWe aimed to determine the association of prenatal exposure to high-molecular-weight phthalates and BPA with pubertal timing in boys and girls participating in the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS) longitudinal cohort study.MethodsWe quantified urinary concentrations of eight phthalate metabolites and BPA at two time points during pregnancy among participating mothers ([Formula: see text]) and conducted clinical Tanner staging of puberty on their children every 9 months between 9 and 13 y of age. We conducted accelerated failure time models and examined the role of child overweight/obese status in this association.ResultsThe sum of urinary metabolites of di(2-ethylhexyl) phthalate [Formula: see text], monobenzyl phthalate (MBzP), and BPA were associated with later onset of at least one of the three outcomes assessed in girls (thelarche, pubarche, or menarche) and with earlier onset of at least one of the two outcomes assessed in boys (gondarche and pubarche). We found that monocarboxynonyl phthalate, monocarboxyoctyl phthalate, mono(3-carboxypropyl) phthalate, and BPA were associated with later pubarche and menarche mostly among normal-weight girls but not overweight/obese girls. MBzP was associated with later thelarche in all girls, and [Formula: see text] was associated with later thelarche and menarche in all girls. BPA and all phthalate biomarkers were associated with earlier gonadarche and pubarche in all boys as well as in overweight/obese boys when stratified by weight. Among normal-weight boys, associations with BPA were also inverse, whereas associations with phthalate metabolites were close to the null or positive.ConclusionsSeveral high-molecular-weight phthalates and BPA were associated with later puberty in girls and earlier puberty in boys included in the CHAMACOS cohort study. Childhood overweight/obesity may modify these associations. https://doi.org/10.1289/EHP3424.

Environmental phenols and parabens are commonly used in personal care products and other consumer products and human exposure to these chemicals is widespread. Although human and animal studies suggest an association between exposure to phenols and parabens and thyroid hormone levels, few studies have investigated the association of in utero exposure to these chemicals and thyroid hormones in pregnant women and their neonates. We measured four environmental phenols (triclosan, benzophenone-3, and 2,4- and 2,5-dichlorophenol), and three parabens (methyl-, propyl-, and butyl paraben) in urine collected from mothers at two time points during pregnancy as part of the CHAMACOS (Center for the Health Assessment of Mothers and Children of Salinas) study. We measured free thyroxine (T4), total T4, and thyroid-stimulating hormone (TSH) in serum of the pregnant women (N = 454) and TSH in their neonates (N = 365). We examined potential confounding by a large number of additional chemical exposures and used Bayesian Model Averaging (BMA) to select the most influential chemicals to include in regression models. We observed negative associations of prenatal urinary concentrations of propyl paraben and maternal TSH (β for two-fold increase = -3.26%, 95% CI: -5.55, -0.90) and negative associations of 2,4-dichlorophenol and maternal free T4 (β for two-fold increase = -0.05, 95% CI: -0.08, -0.02), after controlling for other chemical exposures. We observed negative associations of triclosan with maternal total T4 after controlling for demographic variables, but this association became non-significant after controlling for other chemicals (β for two-fold increase = -0.05, 95% CI: -0.11, 0.00). We found evidence that environmental phenols and parabens are associated with lower TSH and free T4 in pregnant women after controlling for related chemical exposures.

BackgroundAlthough experiments in animals suggest that phthalates may have obesogenic effects, studies on prenatal exposure in children show inconsistent results.MethodsWe measured urinary concentrations of 11 phthalate metabolites collected twice during pregnancy from mothers participating in the Center for the Health Assessment of Mothers and Children of Salinas (CHAMACOS) cohort study (N=345). Height, weight, waist circumference, and percent body fat were assessed in their children between 5 and 12 years of age. We used generalized estimating equations to examine associations at each age and tested for interaction by sex.ResultsMetabolites of diethyl phthalate (DEP), di-n-butyl phthalate (DBP), butyl benzyl phthalate, and di(2-ethylhexyl) phthalate (DEHP) were positively associated with BMI z-score, waist circumference z-score, and percent body fat at multiple ages. At age 12, we observed increased odds of being overweight/obese with each doubling of prenatal concentrations of DEP (odds ratio=1.3; 95% confidence intervals: 1.1, 1.4), DBP (1.2; 1.0, 1.4), and DEHP (1.3; 1.0, 1.6) metabolites. Results were similar in boys and girls except for DBP metabolites and the non-specific metabolite mono-(3-carboxypropyl) phthalate, which showed positive associations only in boys.ConclusionIn utero exposure to certain phthalates is associated with increased BMI and risk for overweight/obesity in childhood.

The opioid crisis is a national health emergency with immense morbidity, mortality, and socioeconomic cost. Emergency department (ED) pain management is tightly linked to the issue of opioid use disorder (OUD), because opioid exposure is necessary for development of OUD. Emergency nurses are on the frontlines of this complex problem, yet little, if any, attention has been paid to the role they play in the prevention and management of either pain or OUD in this unique and important setting. A framework that conceptualizes and optimizes emergency nurses as change agents in the opioid epidemic is urgently needed. While ED pain management and OUD prevention is dependent on the entire care team, this innovative study qualitatively characterizes emergency nurse perceptions of pain management, OUD prevention, and their potential role in each. Content analysis produced 14 categories that were clustered into two themes, "nurses influence ED pain management" and "adjustments in ED pain management", and an overarching message that "pain management depends on the care team." By generating a more comprehensive and nuanced understanding of the role played by emergency nurses, our findings provide essential insights into potential interventions and frameworks. [ABSTRACT FROM AUTHOR]

Over two-thirds of pregnant women in the U.S. have insufficient 25(OH)D (Vitamin D) concentrations, which can adversely impact fetal health. Several pollutants have been associated with 25(OH)D, but have not been considered in the context of chemical co-exposures. We aimed to determine associations between a broad mixture of prenatal environmental chemical exposures and 25(OH)D concentrations in mid-pregnancy. Stored mid-pregnancy serum samples were assayed from 421 women delivering live births in Southern California in 2000–2003. 25(OH)D, six BFRs, eleven polychlorinated biphenyls (PCBs), six per- and polyfluoroalkyl substances, and two organochlorine pesticides were detected in ≥60% of specimens. Gestational exposures to airborne particulate matter ≤ 10 μm (PM 10) and ≤ 2.5 μm (PM 2.5), nitrogen monoxide (NO), nitrogen dioxide (NO 2), and ozone concentrations were derived from monitoring station data. Bayesian Hierarchical Modeling (BHM) and Bayesian Kernel Machine Regression (BKMR) analyses estimated overall mixture and individual chemical associations accounting for co-exposures and covariates with mean 25(OH)D levels, and BHM was used to estimate associations with insufficient (<75 nMol/L) 25(OH)D levels. Non-mixture associations for each chemical were estimated with linear and logistic models. PM 10 [BHM estimate: −0.133 nmol/l 95% Credible Interval (−0.240, −0.026)] was associated with lower 25(OH)D in BHM and BKMR. Higher quantiles of combined exposures were associated with lower 25(OH)D, though with wide credible intervals. In non-mixture models, PM 10 , PM 2.5 , NO, and NO 2 were associated with lower concentrations, while O 3 and PBDE153 were associated with higher 25(OH)D and/or lower insufficiency. While some chemicals were associated with increased and others with decreased 25(OH)D concentrations, the overall mixture was associated with lower concentrations. Mixture analyses differed from non-mixture regressions, highlighting the importance of mixtures approaches for estimating real-world associations. [Display omitted] • Mixture modeling of 30 pollutants in mid-pregnancy and Vitamin D concentrations. • PM 10 was associated with lower Vitamin D. • The overall mixture of pollutant exposure trended with lower Vitamin D. • Non-mixture models showed several air pollutants associated with lower Vitamin D. [ABSTRACT FROM AUTHOR]

Background: Exposure to ambient fine particulate matter (PM2.5) has been linked with premature mortality, but sources of PM2.5 have been less studied.Methods: We evaluated associations between source-specific PM2.5 exposures and cause-specific short-term mortality in eight California locations from 2002 to 2011. Speciated PM2.5 measurements were source-apportioned using Positive Matrix Factorization into eight sources and combined with death certificate data. We used time-stratified case-crossover analysis with conditional logistic regression by location and meta-analysis to calculate pooled estimates.Results: Biomass burning was associated with all-cause mortality lagged 2 days after exposure (lag2) (% changelag2 in odds per interquartile range width increase in biomass burning PM2.5 = 0.8, 95% confidence interval [CI] = 0.2, 1.4), cardiovascular (% changelag2 = 1.3, 95% CI = 0.3, 2.4), and ischemic heart disease (% changelag2 = 2.0, 95% CI = 0.6, 3.5). Vehicular emissions were associated with increases in cardiovascular mortality (% changelag0 = 1.4, 95% CI = 0.0, 2.9). Several other sources exhibited positive associations as well. Many findings persisted during the cool season. Warm season biomass burning was associated with respiratory/thoracic cancer mortality (% changelag1 = 5.9, 95% CI = 0.7, 11.3), and warm season traffic was associated with all-cause (% changelag0 = 1.9, 95% CI = 0.1, 3.6) and cardiovascular (% changelag0 = 2.9, 95% CI = 0.1, 5.7) mortality.Conclusions: Our results suggest that acute exposures to biomass burning and vehicular emissions are linked with cardiovascular mortality, with additional sources (i.e., soil, secondary nitrate, secondary sulfate, aged sea salt, and chlorine sources) showing associations with other specific mortality types. [ABSTRACT FROM AUTHOR]