Sun Y, Headon KS, Umer W
… +11 more, Jiao A, Slezak JM, Avila CC, Chiu VY, Sacks DA, Sanders KT, Molitor J, Benmarhnia T, Chen JC, Getahun D, Wu J
Environ Health Perspect
· 2024 Nov · PMID 39601565
·
Full text
BACKGROUND: Postpartum depression (PPD) has been associated with biological, emotional, social, and environmental factors. However, evidence regarding the effect of temperature on PPD is extremely limited. OBJECTIVES: We...BACKGROUND: Postpartum depression (PPD) has been associated with biological, emotional, social, and environmental factors. However, evidence regarding the effect of temperature on PPD is extremely limited. OBJECTIVES: We aimed to examine the associations between postpartum temperature exposure and PPD. METHODS: We conducted a retrospective cohort study using data from Kaiser Permanente Southern California electronic health records from 1 January 2008 through 31 December 2018. PPD was first assessed using the Edinburgh Postnatal Depression Scale (score ) during the first year of the postpartum period and further identified by using both diagnostic codes and prescription medications. Historical daily ambient temperatures were obtained from the resolution gridMET dataset (https://www.climatologylab.org/gridmet.html) and linked to participants' residential addresses at delivery. Postpartum temperature exposures were measured by calculating various temperature metrics during the period from delivery to PPD diagnosis date. A time-to-event approach with a discrete-time logistic regression was applied to estimate the association between temperature exposure and time to PPD. Effect modification by maternal characteristics and other environmental factors was examined. RESULTS: There were 46,114 (10.73%) PPD cases among 429,839 pregnancies ( age y). Increased PPD risks were positively associated with exposure to higher mean temperature [adjusted odds ratio (aOR) per interquartile range increment: 1.07; 95% confidence interval (CI): 1.05, 1.09] and diurnal temperature range (; 95% CI: 1.06, 1.10); the associations were stronger for maximum temperature compared with minimum temperature. The temperature-related PPD risks were greater among African American, Asian, and Hispanic mothers and among mothers years of age compared with their counterparts. We also observed higher effects of temperature on PPD among mothers exposed to higher air pollution or lower green space levels and among mothers with lower air conditioning penetration rates. CONCLUSION: Maternal exposure to higher temperature and diurnal temperature variability during the postpartum period was associated with an increased risk of PPD. Effect modification by maternal age, race/ethnicity, air pollution, green space, and air conditioning penetration was identified. https://doi.org/10.1289/EHP14783.
Environ Health Perspect
· 2024 Nov · PMID 39585740
·
Full text
High school students and teachers paired with researchers improved awareness, drinking water testing, and abatement in high-risk areas.High school students and teachers paired with researchers improved awareness, drinking water testing, and abatement in high-risk areas.
Yang L, Zhang Y, Hua J
… +11 more, Song G, Li F, Zheng N, Zhang T, Xu Z, Ren X, Zhu B, Han Y, Guo Y, Han J, Zhou B
Environ Health Perspect
· 2024 Nov · PMID 39570742
·
Full text
BACKGROUND: Legacy brominated flame retardants have been recognized as risky factors leading to declined sperm quality. The widespread utilization of decabromodiphenyl ethane (DBDPE) as a replacement for decabromodipheny...BACKGROUND: Legacy brominated flame retardants have been recognized as risky factors leading to declined sperm quality. The widespread utilization of decabromodiphenyl ethane (DBDPE) as a replacement for decabromodiphenyl ether has given rise to considerable concern over its potential risks to reproductive health. OBJECTIVES: The objectives were to quickly determine whether DBDPE affects sperm quality upon exposure, to reveal the reproductive outcomes and underlying molecular mechanisms using an zebrafish model exposed to DBDPE, and to validate the potential impact on DNA damage and energy metabolism balance . METHODS: Zebrafish spermatozoa were treated with DBDPE (0.01, 0.1, 1, ) for 3 h, and the spermatozoa motility and fertilization ability with normal eggs were evaluated. Then adult male zebrafish were treated with DBDPE (0.1, 1, 10, and ) for 2 months, and their reproductive performance was examined. Four-dimensional label-free proteome and phosphoproteome were performed in zebrafish testes, and the findings were validated by multiple indicators. Finally, mouse spermatogonial GC-1 cells were treated with DBDPE (0.1, ) for 72 h, and DNA damage was examined, as well as the energy production of glycolysis and oxidative phosphorylation. RESULTS: exposure to DBDPE caused lower motility and fertilization rates of zebrafish spermatozoa. exposure to DBDPE caused lower sperm motility and abnormal spermatogenesis in male zebrafish testes. Integrated whole-proteome and phosphoproteome analysis revealed DNA damage responses and energy metabolic disorders in zebrafish testes. A dosage window characterized by higher mitochondrial membrane potential (MMP) in combination with unchanged reactive oxygen species and apoptosis rates was observed in both zebrafish testes and GC-1 cells. DISCUSSION: This study suggests that in zebrafish, DBDPE exposure could impair sperm quality and spermatogenesis, and the underlying mechanism could be related to DNA damage and energy metabolic reprogramming in testicular germ cells. https://doi.org/10.1289/EHP14426.
Environ Health Perspect
· 2024 Nov · PMID 39570741
·
Full text
A state-of-the-science review probed whether biodiversity inside the body and in the environment were associated with certain immune responses.A state-of-the-science review probed whether biodiversity inside the body and in the environment were associated with certain immune responses.
James-Todd T, Tomsho KS, Gaston SA
… +2 more, Elliott KC, Jackson CL
Environ Health Perspect
· 2024 Nov · PMID 39541091
·
Full text
BACKGROUND: In environmental epidemiology, we use an array of tools from various, related disciplines to answer key questions about environmental exposures in relation to health outcomes. Typically, we ask questions rela...BACKGROUND: In environmental epidemiology, we use an array of tools from various, related disciplines to answer key questions about environmental exposures in relation to health outcomes. Typically, we ask questions related to what, who, where, when, and how. We value these questions because they contribute to novel scientific discovery and our understanding of disease etiology linked to environmental exposures. In addition, these questions help us better understand who might be at highest risk of exposure and subsequent risk of disease. Although necessary for the goals of environmental epidemiology, these questions are insufficient for addressing environmental health disparities. Specifically, these questions may be able to help us describe exposure-health outcome associations but are limited in their ability to move beyond identification to intervening on observed disparities to achieve environmental health equity. OBJECTIVES: We sought to emphasize the need to value and routinely add the key question of "Why?" in environmental epidemiological studies. In asking this additional critical question, we can identify and incorporate the structural determinants and drivers of environmental exposure disparities and determine whether these factors are linked to existing and historically recalcitrant health disparities. Further, we can design effective studies that build on existing frameworks to address the fundamental causes of environmental health disparities. DISCUSSION: This commentary underscores the need to routinely incorporate "why" questions in the practice of environmental epidemiology. By asking and addressing "Why?" we can employ better, more solution-oriented study designs, improve data collection, and enhance our ability to collaborate with diverse study populations through trust-building and community-engaged research. Incorporating these approaches will move environmental epidemiology forward from mostly documenting to actively addressing environmental health disparities. https://doi.org/10.1289/EHP14513.
Liu Y, Ma X, Le Y
… +4 more, Feng J, Xu M, Wang W, Wang C
Environ Health Perspect
· 2024 Nov · PMID 39514743
·
Full text
BACKGROUND: Environmental chemical exposures have been associated with metabolic outcomes, and typically, their binding to nuclear hormone receptors is considered the molecular initiating event (MIE) for a number of outc...BACKGROUND: Environmental chemical exposures have been associated with metabolic outcomes, and typically, their binding to nuclear hormone receptors is considered the molecular initiating event (MIE) for a number of outcomes. However, more studies are needed to understand the influence of such exposures on cell membrane-bound adiponectin receptors (AdipoRs), which are critical metabolic regulators. OBJECTIVE: We aimed to clarify the potential interactions between AdipoRs and environmental chemicals, specifically organophosphorus flame retardants (OPFRs), and the resultant effects. METHODS: Employing simulation, cell thermal shift, and noncompetitive binding assays, we screened eight OPFRs for interactions with AdipoR1 and AdipoR2. We tested two key events underlying AdipoR modulation upon OPFR exposure in a liver cell model. The Toxicological Prioritization Index (ToxPi)scoring scheme was used to rank OPFRs according to their potential to disrupt AdipoR-associated metabolism. We further examined the inhibitory effect of OPFRs on AdipoR signaling activation in mouse models. RESULTS: Analyses identified pi-pi stacking and pi-sulfur interactions between the aryl-OPFRs 2-ethylhexyl diphenyl phosphate (EHDPP), triphenyl phosphate (TPhP), and tricresyl phosphate (TCP) and the transmembrane cavities of AdipoR1 and AdipoR2. Cell thermal shift assays showed a rightward shift in the AdipoR proteins' melting curves upon exposure to these three compounds. Although the binding sites differed from adiponectin, results suggest that aryl-OPFRs noncompetitively inhibited the binding of the endogenous peptide ligand ADP355 to the receptors. Analyses of key events underlying AdipoR modulation revealed that glucose uptake was notably lower, whereas lipid content was higher in cells exposed to aryl-OPFRs. EHDPP, TCP, and TPhP were ranked as the top three disruptors according to the ToxPi scores. A noncompetitive binding between these aryl-OPFRs and AdipoRs was also observed in wild-type (WT) mice. In db/db mice, the finding of lower blood glucose levels after ADP355 injection was diminished in the presence of a typical aryl-OPFR (TCP). WT mice exposed to TCP demonstrated lower AdipoR1 signaling, which was marked by lower phosphorylated AMP-activated protein kinase (pAMPK) and a higher expression of gluconeogenesis-related genes. Moreover, WT mice exposed to ADP355 demonstrated higher levels of pAMPK protein and peroxisome proliferator-activated receptor- messenger RNA. This was accompanied by higher glucose disposal and by lower levels of long-chain fatty acids and hepatic triglycerides; these metabolic improvements were negated upon TCP co-treatment. CONCLUSIONS: , , and assays suggest that aryl-OPFRs act as noncompetitive inhibitors of AdipoRs, preventing their activation by adiponectin, and thus function as antagonists to these receptors. Our study describes a novel MIE for chemical-induced metabolic disturbances and highlights a new pathway for environmental impact on metabolic health. https://doi.org/10.1289/EHP14634.
Environ Health Perspect
· 2024 Nov · PMID 39514742
·
Full text
The integrated approach tackles a perfect storm of poverty, invasive rats, deforestation, and climate change that is contributing to the increase in bubonic plague cases.The integrated approach tackles a perfect storm of poverty, invasive rats, deforestation, and climate change that is contributing to the increase in bubonic plague cases.
Watanabe D, Maruyama K, Tamakoshi A
… +2 more, Muraki I, JACC Study Group
Environ Health Perspect
· 2024 Nov · PMID 39509283
·
Full text
BACKGROUND: Planetary and human health are highly intertwined; our current food system is associated with high greenhouse gas emissions (GHGE) and burden of disease. OBJECTIVE: The aim of this study was to investigate th...BACKGROUND: Planetary and human health are highly intertwined; our current food system is associated with high greenhouse gas emissions (GHGE) and burden of disease. OBJECTIVE: The aim of this study was to investigate the associations of diet-related GHGE with all-cause and cause-specific mortality in Japan. METHODS: This study included 58,031 Japanese adults (35,078 women and 22,953 men) 40-79 y of age who participated in the Japan Collaborative Cohort Study during the period 1988-1990. Diet-related GHGE was calculated from dietary intake estimated by a validated food frequency questionnaire and previously developed GHGE tables of each food and beverage. Participants were classified into quintiles of diet-related GHGE per kg food/d. Hazard ratios (HRs) of all-cause and cause-specific mortality were calculated using the Cox proportional hazard and restricted cubic spline models. RESULTS: The average diet-related GHGE was . Over a period of 19.3 y (955,819 person-years) of median follow-up, 11,508 deaths were documented. After adjusting for lifestyle and medical history, in comparison with the fourth quintiles of diet-related GHGE, the first and fifth quintiles were associated with a higher risk of all-cause mortality: multivariable HR of all-cause mortality was 1.11 [95% confidence interval (CI): 1.05, 1.18] and 1.09 (95% CI: 1.03, 1.17) for the lowest and highest GHGE, respectively; those of cardiovascular disease mortality were 1.23 (95% CI: 1.10, 1.38) and 1.22 (95% CI: 1.08, 1.37), respectively. The diet-related GHGE range with the lowest HR of all-cause mortality was food/d ( for nonlinearity ). Replacing one serving of red meat with one serving of pulses was inversely associated with all-cause mortality (; 95% CI: 0.93, 0.99) and GHGE (mean change, ; 95% CI: , ). DISCUSSION: Diet-related GHGE was associated with all-cause and cardiovascular disease mortality in a U-shaped fashion. This finding could be useful for creating a policy for sustainable shifts in dietary habits that will benefit the population and environmental health. https://doi.org/10.1289/EHP14935.
Tan Y, Eick SM, Dunlop AL
… +11 more, Barr DB, Taibl KR, Steenland K, Kannan K, Robinson M, Chang CJ, Panuwet P, Yakimavets V, Marsit CJ, Ryan PB, Liang D
Environ Health Perspect
· 2024 Nov · PMID 39504273
·
Full text
BACKGROUND: Longitudinal trends in per- and polyfluoroalkyl substances (PFAS) serum concentrations across pregnancy have not been thoroughly examined, despite evidence linking prenatal PFAS exposures with adverse birth o...BACKGROUND: Longitudinal trends in per- and polyfluoroalkyl substances (PFAS) serum concentrations across pregnancy have not been thoroughly examined, despite evidence linking prenatal PFAS exposures with adverse birth outcomes. OBJECTIVES: We sought to characterize longitudinal PFAS concentrations across pregnancy and to examine the maternal-fetal transfer ratio among participants in a study of risk and protective factors for adverse birth outcomes among African Americans. METHODS: In the Atlanta African American Maternal-Child cohort (2014-2020), we quantified serum concentrations of four PFAS in 376 participants and an additional eight PFAS in a subset of 301 participants during early (8-14 weeks gestation) and late pregnancy (24-30 weeks gestation). Among these, PFAS concentrations were also measured among 199 newborns with available dried blood spot (DBS) samples. We characterized the patterns, variability, and associations in PFAS concentrations at different time points across pregnancy using intraclass correlation coefficients (ICCs), maternal-newborn pairs transfer ratios, linear mixed effect models, and multivariable linear regression, adjusting for socioeconomic and prenatal predictors. RESULTS: Perfluorohexane sulfonic acid (PFHxS), perfluorooctane sulfonic acid (PFOS), perfluorooctanoic acid (PFOA), and perfluorononanoic acid (PFNA) were detected in of maternal samples, with PFHxS and PFOS having the highest median concentrations. We observed high variability in PFAS concentrations across pregnancy time points (). All median PFAS concentrations increased from early to late pregnancy, except for PFOA and N-methyl perfluorooctane sulfonamido acetic acid (NMFOSAA), which decreased [paired -test for all PFAS except for PFOA and perfluorobutane sulfonic acid (PFBS)]. Prenatal serum PFAS were weakly to moderately correlated with newborn DBS PFAS ( ). The median maternal-fetal PFAS transfer ratio was lower for PFAS with longer carbon chains. After adjusting for socioeconomic and prenatal predictors, in linear mixed effect models, the adjusted mean PFAS concentrations significantly increased during pregnancy, except for PFOA. In multivariable linear regression, PFAS concentrations in early pregnancy significantly predicted the PFAS concentrations in late pregnancy and in newborns. DISCUSSION: We found that the concentrations of most PFAS increased during pregnancy, and the magnitude of variability differed by individual PFAS. Future studies are needed to understand the influence of within-person PFAS variability during and after pregnancy on birth outcomes. https://doi.org/10.1289/EHP14334.
Environ Health Perspect
· 2024 Nov · PMID 39495174
·
Full text
Gut microbes appeared to play a role in the obesity outcomes observed in mice fed manufactured polystyrene microspheres.Gut microbes appeared to play a role in the obesity outcomes observed in mice fed manufactured polystyrene microspheres.
Sukumaran K, Botternhorn KL, Schwartz J
… +9 more, Gauderman J, Cardenas-Iniguez C, McConnell R, Hackman DA, Berhane K, Ahmadi H, Abad S, Habre R, Herting MM
Environ Health Perspect
· 2024 Oct · PMID 39475730
·
Full text
BACKGROUND: Emerging literature suggests that fine particulate matter [with aerodynamic diameter ()] air pollution and its components are linked to various neurodevelopmental outcomes. However, few studies have evaluate...BACKGROUND: Emerging literature suggests that fine particulate matter [with aerodynamic diameter ()] air pollution and its components are linked to various neurodevelopmental outcomes. However, few studies have evaluated how component mixtures from distinct sources relate to cognitive outcomes in children. OBJECTIVES: This cross-sectional study investigated how ambient concentrations of component mixtures relate to neurocognitive performance in 9- to 10-year-old children, as well as explored potential source-specific effects of these associations, across the US. METHODS: Using spatiotemporal hybrid models, annual concentrations of 15 chemical components of were estimated based on the residential address of child participants from the Adolescent Brain Cognitive Development (ABCD) Study. General cognitive ability, executive function, and learning/memory scores were derived from the NIH Toolbox. We applied positive matrix factorization to identify six major sources based on the 15 components, which included crustal, ammonium sulfate, biomass burning, traffic, ammonium nitrate, and industrial/residual fuel burning. We then utilized weighted quantile sum (WQS) and linear regression models to investigate associations between components' mixture, their potential sources, and children's cognitive scores. RESULTS: Mixture modeling revealed associations between cumulative exposure and worse cognitive performance across all three outcome domains, including shared overlap in detrimental effects driven by ammonium nitrates, silicon, and calcium. Using the identified six sources of exposure, source-specific negative associations were identified between ammonium nitrates and learning & memory, traffic and executive function, and crustal and industrial mixtures and general cognitive ability. Unexpected positive associations were also seen between traffic and general ability as well as biomass burning and executive function. DISCUSSION: This work suggests nuanced associations between outdoor exposure and childhood cognitive performance, including important differences in cognition related both to individual chemicals as well as to specific sources of these exposures. https://doi.org/10.1289/EHP14418.
Environ Health Perspect
· 2024 Oct · PMID 39475729
·
Full text
BACKGROUND: Scientists who communicate societally relevant information face challenging contexts in which misinformation, disinformation, hype, and spin are prevalent. As a result, they often face difficult decisions abo...BACKGROUND: Scientists who communicate societally relevant information face challenging contexts in which misinformation, disinformation, hype, and spin are prevalent. As a result, they often face difficult decisions about how to frame their work in a socially responsible manner. OBJECTIVES: Drawing from the literature on science communication and framing, we identify tradeoffs that environmental health scientists face when deciding how to communicate their work, and we propose strategies for handling these tradeoffs. We use research on the human health effects of environmental endocrine disruptors as a case study to illustrate these challenges and strategies. DISCUSSION: We examine four major frames (i.e., ways of packaging information that draw attention to facets of an issue or topic) in discussions of the effects of endocrine-disrupting chemicals on sexual and neural development and obesity. We show how these frames can be beneficial (e.g., focusing public attention on environmental health threats and promoting actions to address environmental pollution) while simultaneously having harmful effects (e.g., contributing to stigmatization of particular groups or the promotion of harmful political ideologies). CONCLUSIONS: Researchers who seek to responsibly communicate societally relevant work can employ several strategies to mitigate difficult tradeoffs, including ) striving for sensitivity to the social context and its relationship to their framing choices, ) choosing to avoid some frames, ) employing frames that alleviate ethical tensions, ) fostering education to alleviate harms, ) developing interdisciplinary and community collaborations, and ) working with institutions like scientific societies and journals to develop guidance on responsible communication practices. https://doi.org/10.1289/EHP14527.
Environ Health Perspect
· 2024 Oct · PMID 39450969
·
Full text
Exposures to chemicals, including phthalates, triphenyl phosphate, and dibutyl phosphate, have been associated with increased levels of lipid markers, such as elevated low-density lipoprotein.Exposures to chemicals, including phthalates, triphenyl phosphate, and dibutyl phosphate, have been associated with increased levels of lipid markers, such as elevated low-density lipoprotein.