Journal of Exposure Science and Environmental Epidemiology最新文献

Background: Lead exposure remains a key problem for children during development. One treatment for lead poisoning is chelation - a topic that remains controversial with varied results. Bone lead serves as a marker of total body burden of lead and encompasses between 60-90% of lead storage in children.

Objective: In this study, we aimed to identify the change in bone lead as a result of chelation therapy in a group of lead poisoned children (blood lead >25 µg/dL).

Methods: Upon diagnosis with lead poisoning at Xinhua Hospital in Shanghai, China, children were recruited to our study, had their bone lead levels measured, and underwent one-week of intravenous, in-patient ethylenediaminetetraacetic acid chelation treatment. Up to three clinical visits with the same treatment protocol and bone lead measurements were completed over the two-year study. We measured biomarkers of lead exposure for children exposed via various potential sources, including home contaminants, local industrial emissions, traditional medicines, or lead cookware.

Results: We observed significant differences with bone lead after chelation therapy (p < 0.0001), even after calculating a conservative model for theoretical decay from known bone turnover (p = 0.01). The difference identified between our observed change in bone lead and literature established bone lead change significantly increased with more chelation treatments. A significant reduction in bone lead was observed following chelation treatment of children with lead poisoning - a difference that increased more with more chelation.

Significance: Study results indicate that chelation treatment is effective in reducing bone lead stores in children with initial blood lead levels greater than 25 µg/dL.

Impact statement: Lead exposure in children is a consistent problem - drastically impacting health across the life span. After exposure, lead stores in the bone of children serving as a potential endogenous source of exposure for years to decades. Our study demonstrated that chelation therapy, while reducing blood lead levels, additionally reduced bone lead levels. A reduction in bone lead would effectively reduce the potential for endogenous release of lead and restrict the damage done by lead exposure.

Background: Noise exposure and lower socioeconomic status (SES) are both independently linked to increased cardiovascular disease (CVD) risk. Although these factors frequently coexist, their combined impact and the underlying pathophysiological mechanisms remain poorly understood.

Objectives: This study aimed to evaluate the joint effects of high transportation noise exposure and lower SES on major adverse cardiovascular events (MACE) and the role of the neural-arterial axis in mediating this relationship.

Methods: We retrospectively analyzed data from 507 individuals who underwent clinical ¹⁸F-FDG-PET/CT imaging at a single center. SES was evaluated using local median income (as a primary measure) and area deprivation index (ADI, as a secondary measure). Participants were classified into three groups based on transportation noise exposure and income/ADI: low noise/higher SES, high noise or lower SES, and high noise/lower SES. Cox models assessed MACE risks. Linear regression models evaluated associations with stress-related neural activity (SNA) and arterial inflammation (ArtI).

Results: The combination of high noise exposure and low income (vs. neither exposure) associated with increased MACE risk (HR [95% CI]: 5.597 [2.201-14.233], p < 0.001). SNA (standardized β [95% CI]: 0.389 [0.192-0.586], p < 0.001) and ArtI (0.151 [0.005-0.298], p = 0.043) were greater in this group. Mediation analysis showed that the neural-arterial axis contributes to increased exposure-related MACE risk and accounts for 8% of the overall effect. Similar results were found with ADI.

Impact statement: Our study uniquely demonstrates how combined high transportation noise and lower socioeconomic status additively increases cardiovascular disease risk through specific biological pathways, particularly via effects on stress-associated neural activity and arterial inflammation. As such, the research offers novel insights into the interplay between environmental and socioeconomic factors in cardiovascular health. This underscores an urgent need for integrated public health strategies that address both noise pollution and socioeconomic disparities and provides a foundation for targeted interventions aimed at reducing the burden of cardiovascular disease in vulnerable populations. Central illustration of hypothesized mechanistic pathways linking transportation noise/SES exposure groups and MACE. SNA stress related neural activity (as AmygAc-ratio of amygdala to background cortical activity), MACE major adverse cardiovascular events, ArtI arterial inflammation, ADI Area Deprivation Index, SES socioeconomic status.

Background: Prenatal air pollution (AP) exposure has been linked to postpartum psychological functioning, impacting health outcomes in both women and children. Extant studies primarily focused on individual pollutants.

Objective: To assess the association between prenatal exposure to a mixture of seven AP components and postpartum psychological functioning using daily exposure data and data-driven statistical methods.

Methods: Analyses included 981 women recruited at 24.0 ± 9.9 weeks gestation and followed longitudinally. We estimated prenatal daily exposure levels for constituents of fine particles [elemental carbon (EC), organic carbon (OC), nitrate (NO₃^-), sulfate (SO₄^2-), ammonium (NH₄⁺)], nitrogen dioxide (NO₂), and ozone (O₃) using validated global 3-D chemical-transport models and satellite-based hybrid models based on residential addresses. Edinburgh Postnatal Depression Scale (EPDS) was administered to participants to derive a total EPDS score and the subconstruct scores for anhedonia and depressive symptoms. A distributed lag model (DLM) was employed within Bayesian Kernel Machine Regression (BKMR) to develop time-weighted exposure profile for each pollutant. These exposures were then input into a Weighted Quantile Sum (WQS) regression to estimate an overall mixture effect, adjusted for maternal age, education, race/ethnicity, season of delivery, and delivery year. Effect modification by race/ethnicity and fetal sex was also examined.

Results: Women were primarily Hispanic (51%) and Black (32%) reporting ≤12 years of education (58%). Prenatal exposure to an AP mixture was significantly associated with increased anhedonia subscale z-scores, particularly in Hispanics (β = 0.07, 95%CI = 0.004-0.13, per unit increase in WQS index). It was also borderline associated with increased total EPDS (β = 0.11, 95%CI = 0.00-0.22) and depressive symptom subscale (β = 0.09, 95%CI = -0.02 to 0.19) z-scores, particularly among Hispanic women who gave birth to a male infant. Sulfate (SO₄^2-), O₃ and OC were major contributors to these associations.

Impact: This study utilizes an advanced data-driven approach to examine the temporally- and mixture-weighted effects of prenatal air pollution exposure on postpartum psychological functioning. We found that exposure to a prenatal air pollution mixture predicted poorer postpartum psychological functioning, particularly anhedonia symptoms in Hispanic women. Findings underscore the importance of considering both exposure mixtures as well as potential modifying factors to better help identify particular pollutants that drive effects and susceptible populations, which can inform more effective intervention strategies.

Background: Knowledge of relationships between tropospheric ozone and mental and developmental health outcomes is currently inconclusive, with the largest knowledge gaps for children. This gap is important to address as evidence suggests that climate change will worsen ozone pollution.

Objective: We examine the association of average ozone exposure during the preconception period, and first, second and third trimesters of pregnancy on the odds of intellectual disability (ID) in Utah children.

Methods: For the period of 2002-2020, we assembled daily, tract-level ozone concentration data, data on ID case status, and data on cases' full siblings and population controls. We analyzed the data using generalized estimating equations.

Results: Ozone was positively associated with the odds of ID in cases vs. their siblings (in the preconception, first, second and third trimester exposure windows, all p < 0.05, n = 1042) and vs. population controls (only in the second trimester exposure window, p < 0.05, n = 5179). The strength of the association was largest during the second trimester in both analyses. A second trimester average ozone level increase of 10 ppb was associated with a 55.3% increase in the odds of ID relative to full siblings (95% confidence interval [CI]: 1.171-2.058) and a 22.8% increase in the odds of ID relative to population controls (CI: 1.054-1.431). Findings were robust to different subsets of sibling controls as well as several sensitivity analyses.

Significance: Results document that ozone has a measurable relationship with children's cognitive development in Utah.

Impact statement: Evidence suggests that climate change will worsen ozone pollution. The potential amplifying effect of climate change on ozone is more certain than it is for fine particulate matter. This means that ozone and health research will remain relevant into the future. Currently, several systematic reviews and meta-analyses have concluded that knowledge about ozone and cognitive health is insufficient, especially for children. Using two different study designs, we find that prenatal ozone exposure is associated with risk of intellectual disability in children.

Exposure science plays an essential role in the U.S. Environmental Protection Agency's (U.S. EPA) mission to protect human health and the environment. The U.S. EPA's Center for Public Health and Environmental Assessment (CPHEA) within the Office of Research and Development (ORD) provides the exposure science needed to characterize the multifaceted relationships between people and their surroundings in support of national, regional, local and individual-level actions. Furthermore, exposure science research must position its enterprise to tackle the most pressing public health challenges in an ever-changing environment. These challenges include understanding and confronting complex human disease etiologies, disparities in the social environment, and system-level changes in the physical environment. Solutions will sustainably balance and optimize the health of people, animals, and ecosystems. Our objectives for this paper are to review the role of CPHEA exposure science research in various recent decision-making contexts, to present current challenges facing U.S. EPA and the larger exposure science field, and to provide illustrative case examples where CPHEA exposure science is demonstrating the latest methodologies at the intersection of these two motivations. This blueprint provides a foundation for applying exposomic tools and approaches to holistically understand real-world exposures so optimal environmental public health protective actions can be realized within the broader context of a One Health framework. IMPACT STATEMENT: The U.S. EPA's Center for Public Health and Environmental Assessment exposure research priorities reside at the intersection of environmental decision contexts and broad public health challenges. The blueprint provides a foundation for advancing the tools and approaches to holistically understand real-world exposures so optimal environmental protection actions can be realized. A One Health lens can help shape exposure research for maximum impact to support solutions that are transdisciplinary and must engage multiple sectors.

Background: Exposure to ambient air pollution is associated with morbidity and mortality, making it an important public health concern. Emissions from motorized traffic are a common source of air pollution but evaluating the contribution of traffic-related air pollution (TRAP) emissions to health risks is challenging because it is difficult to disentangle the contribution of individual air pollution sources to exposure contrasts in an epidemiological study.

Objective: This paper describes a new framework to identify whether air pollution differences reflect contrasts in TRAP exposures. Because no commonly measured pollutant is entirely specific to on-road motor vehicles, this exposure framework combined information on pollutants, spatial scale (i.e., geographic extent), and exposure assessment methods and their spatial scale to determine whether the estimated effect of air pollution in a given study was related to differences in TRAP.

Methods: The exposure framework extended beyond the near-road environment to include differences in exposure to TRAP at neighborhood resolution ( ≤ 5 km) across urban, regional, and national scales. It also embedded a stricter set of criteria to identify studies that provided the strongest evidence that exposure contrasts were related to differences in traffic emissions.

Results: Application of the framework to the transparent selection of epidemiological studies for a systematic review produced insights on assessing and improving comparability of TRAP exposure measures, particularly for indirect measures such as distances from roads. It also highlighted study design challenges related to the duration of measurements and the structure of epidemiological models.

Impact statement: This manuscript describes a new exposure framework to identify studies of traffic-related air pollution, a case study of its application in an HEI systematic review, and its implications for exposure science and air pollution epidemiology experts. It identifies challenges and provides recommendations for the field going forward. It is important to bring this information to the attention of researchers in air pollution exposure science and epidemiology because applying the broader lessons learned will improve the conduct and reporting of studies going forward.

Background: Cooking-related emissions contribute to air pollutants in the home and may influence children's health outcomes.

Objective: In this pilot study, we investigate the effects of a cooking ventilation intervention in homes with gas stoves, including a video-based educational intervention and range hood replacement (when needed) in children's homes.

Methods: This was a pilot (n = 14), before-after trial (clinicaltrials.gov #NCT04464720) in homes in the San Francisco Bay Area that had a school-aged child, a gas stove, and either a venting range hood or over-the-range microwave/hood. Cooking events, ventilation use, and indoor air pollution were measured in homes for 2-4 weeks, and children completed respiratory assessments. Midway, families received this intervention: (1) education about the hazards of cooking-related pollutants and benefits of both switching to back burners and using the range hood whenever cooking and (2) ensuring the range hood met airflow and sound performance standards. The educational intervention was delivered via a video developed in conjunction with local youth.

Results: We found substantially increased use of back burners and slight increases in range hood use during cooking after intervening. Even though there was no change in cooking frequency or duration, these behavior changes resulted in decreases in nitrogen dioxide (NO2), including significant decreases in the total integrated concentration of NO2 over all cooking events from 1230 ppb*min (IQR 336, 7861) to 756 (IQR 84.0, 4210; p < 0.05) and NO2 collected on samplers over the entire pre- and post-intervention intervals from 10.4 ppb (IQR 3.5, 47.5) to 9.4 (IQR 3.0, 36.1; p < 0.005). There were smaller changes in PM2.5, and no changes were seen in respiratory outcomes.

Impact: This pilot before-after trial evaluated the use of a four-minute educational video to improve cooking ventilation in homes with gas stoves and one or more school-aged children. Participant behavior changed after watching the video, and there were decreases in indoor air pollutant concentrations in the home, some of which were significant. This brief video is now publicly available in English and Spanish (wspehsu.ucsf.edu/projects/indoor-air-quality), and this provides suggestive evidence of the utility of this simple intervention, which could be particularly beneficial for households that have children with asthma.

Background: Endogenous and exogenous hormones may be present in beef. Human consumption of hormones has been linked to adverse health effects.

Objective: To estimate daily intake of hormonal growth promotants (HGP) from beef consumed by the US population.

Methods: We combined self-reported beef consumption information from a nationally-representative survey with concentrations of 12 HGP measured in 397 samples of retail beef/fat purchased in California. We defined typical, high, and maximum intake scenarios assuming self-reported consumed beef contained the mean, 95^th percentile, and maximum concentrations of each HGP, respectively. We estimated distributions of usual (i.e., long-term) daily intake and short-term daily intake (µg/kg/day). We calculated the hazard quotient (HQ), or ratio of estimated intake to the World Health Organization's acceptable daily intake (ADI) for the HGP.

Results: The highest estimated HQs were found for melengestrol acetate (MGA). For usual daily intake under the typical intake scenario, no HQ exceeded 0.02 (0.00047 µg MGA/kg/day). Under the maximum intake scenario, the highest HQ was 0.29 (0.0087 µg MGA/kg/day), corresponding to the 99^th percentile of intake among young boys (ages 1-5). The highest short-term intake estimates for MGA under the maximum intake scenario were the 99^th percentile of intake among young girls and boys, which equaled (HQ = 1.00) or exceeded (HQ = 1.29) the ADI for MGA, respectively.

Impact: Hormonal growth promotants (HGP) are used to increase beef production and have been linked to adverse reproductive effects. We estimated daily intake of MGA and several other HGP using US nationally-representative beef consumption data collected between 2015-2018 and HGP concentrations in retail beef. Estimated intake was highest for young children, but estimates were generally very low compared to current health-based intake limits. However, these limits are typically based on studies in adult animals, and further study of potential adverse effects during sensitive developmental periods, such as in early life, may be warranted to ensure recommended intake limits are health-protective.

Background: The epidemiological evidence regarding the correlation between air pollution, residential greenspace, and the risk of kidney stone disease (KSD) is limited, with no large-scale prospective studies conducted on this relationship.

Objective: We conducted a large-scale prospective study from the UK Biobank to explore the correlation between air pollution, residential greenspace, and the risk of KSD.

Methods: This study included 419,835 UK Biobank participants who did not have KSD at baseline. An air pollution score was derived through the summation of concentrations for five air pollutants, including particulate matter (PM) with aerodynamic diameter ≤2.5 μm (PM_2.5), ranging from 2.5 to 10 μm (PM_2.5-10), ≤10 μm (PM₁₀), nitrogen dioxide (NO₂), and nitrogen oxides (NO_x). Various covariates were adjusted for in Cox proportional hazard regression to evaluate the risk of KSD associated with air pollution score, single air pollutant, and residential greenspace.

Results: During a follow-up period of 12.7 years, 4503 cases of KSD were diagnosed. Significant associations were found between KSD risk and air pollution score (HR: 1.08, 95% CI: 1.03-1.13), PM_2.5 (1.06, 1.02-1.11), PM₁₀ (1.04, 1.01-1.07), NO₂ (1.09, 1.02-1.16), NO_x (1.08, 1.02-1.11), greenspace buffered at 300 m (0.95, 0.91-0.99), and greenspace buffered at 1000 m (0.92, 0.86-0.98) increase per interquartile range (IQR). PM_2.5 and NO₂ reductions may be a key mechanism for the protective impact of residential greenspace on KSD (P _{for indirect path} < 0.05).

Impact: Prolonged exposure to air pollution was correlated with a higher risk of KSD, while residential greenspace exhibits an inverse association with KSD risk, partially mediated by the reduction in air pollutants concentrations. These findings emphasize the significance of mitigating air pollution and maintaining substantial greenspace exposure as preventive measures against KSD.