Environmental Health最新文献

Background: Zearalenone (ZEN), a secondary metabolite of Fusarium fungi, is one of the most common mycotoxins in global food supplies such as cereal grains and processed food. ZEN and its metabolites are commonly referred to as mycoestrogens, due to their ability to directly bind nuclear estrogen receptors α (ER-α) and β (ER-β). Zeranol, a synthetic mycoestrogen, is administered to U.S. cattle as a growth promoter. Despite widespread human exposure and ample evidence of adverse reproductive impacts in vitro and in vivo, there has been little epidemiological research on the health impacts of ZEN exposure during pregnancy. The objective of our study was to examine associations between ZEN and gestational weight gain (GWG).

Methods: Urine samples were collected in each trimester from pregnant participants in the UPSIDE cohort (n = 286, Rochester, NY, USA). High performance liquid chromatography and high-resolution tandem mass spectrometry were used to quantify concentrations of ZEN as well as ∑mycoestrogens (composite sum of ZEN metabolites; ng/ml). Maternal weights at clinical visits were abstracted from medical records. We fitted longitudinal models of specific-gravity adjusted, log-transformed ZEN and ∑mycoestrogens in relation to total GWG (kilograms) and GWG rate (kilograms/week). We additionally examined risk of excessive GWG (in relation to Institute of Medicine guidelines) and considered effect modification by fetal sex.

Results: ZEN and ∑mycoestrogens were detected in > 93% and > 95% of samples, respectively. Mycoestrogen concentrations were positively associated with total GWG (ZEN β:0.50 kg; 95%CI: 0.13, 0.87) and GWG rate (ZEN β:0.20 kg/week; 95%CI: 0.01, 0.03). Associations tended to be stronger among participants carrying male (versus female) fetuses and results were robust to adjustment for diet.

Conclusions: Mycoestrogen exposure during pregnancy may contribute to greater GWG. Future research is needed to understand potential influences on downstream maternal and offspring health.

Background: Neonicotinoid pesticides ('neonics') - imidacloprid, thiamethoxam, clothianidin, acetamiprid, dinotefuran-are the most widely used class of insecticides in the world. They have a neurotoxic mechanism of action, similar to nicotine. They are detected in food, waterways, tap water, and breast milk.

Methods: We make use of the non-occupational human pesticide poisoning reports in the U.S. Environmental Protection Agency (EPA) online Incident Data System (IDS). The data set contains individual incidents, and incidents aggregated and submitted in bulk to EPA. IDS reports are predominantly self-reported information of varying and often low level of detail and are not routinely validated or verified by EPA.

Results: We reviewed 842 non-occupational human poisoning incidents associated with neonics in the IDS from 2018 through 2022. There are four human fatality reports, two associated with clothianidin and two with acetamiprid. Major illnesses such as seizures were reported in several cases, including with dinotefuran cockroach bait product, and an imidacloprid lawn product. Moderate poisonings make up 88% of the total poisonings (740 of 842), with most of those associated with imidacloprid (547 incidents) or dinotefuran (102 incidents). Common reported symptoms classified as moderate often included two or more of the following: headaches; dizziness; lethargy; eye or throat irritation; skin itching and rash; chemical burns and skin peeling; face swelling; muscle weakness or tremors; vomiting; diarrhea; pain and tightness in chest; open sores; and general pain. These incidents stem mainly from residential uses, such as lawn and garden insect repellents, home pest treatments for bed bugs or roaches, and products used to treat pets for fleas and ticks.

Conclusion: Given the evidence of neurotoxicity, EPA should use its legal authority to cancel unsafe products and unnecessary uses - including from seed treatments, and residential pet and lawncare products - to prevent further human suffering.

Background: A growing body of epidemiologic and toxicologic literature indicates that fine airborne particulate matter (PM_2.5) pollution is neurotoxic and threatens children's neurobehavioral development, resulting in reduced cognitive function. Understanding the magnitude of this effect is critical for establishing public health policies that will protect children's health, preserve human capital, and support societal progress.

Objective: To quantify the association between ambient PM_2.5 air pollution and loss of cognitive function in children, as measured by Intelligence Quotient (IQ) scores, through a systematic literature review and meta-analysis.

Methods: Following PRISMA guidelines, we conducted a systematic literature search across seven databases: Agricultural and Environmental Science, BIOSIS Citation Index, Embase, GreenFILE, PubMed, Scopus, and Web of Science to identify original scientific studies that investigated the impact of PM_2.5 exposure during pre-and postnatal periods on IQ loss during childhood. Using data from studies included for final review, we conducted a meta-analysis, using a random effects model to compute a beta coefficient that quantifies the overall effect of PM_2.5 exposure on Full-Scale IQ (FSIQ), Performance IQ (PIQ), and Verbal IQ (VIQ).

Findings: Of the 1,107 unique publications identified, six studies met the inclusion criteria for final review, representing 4,860 children across three continents (North America, Europe, and Asia). The mean PM_2.5 concentration across all studies was 30.4 ± 24.4 µg/m³. Exposure timing ranged from the prenatal period to mid-childhood. Children were an average of 8.9 years old at the time of cognitive testing. We found that each 1 µg/m³ increase in PM_2.5 concentration is associated with a -0.27 point change in FSIQ (p < 0.001), 0.39 point change in PIQ (p = 0.003), and -0.24 point change in VIQ (p = 0.021).

Conclusion: Through a systematic review and meta-analysis, we identified a statistically significant relationship between increased exposure to PM_2.5 air pollution and reduced cognitive function in children, with the most pronounced impact on PIQ. This analysis will enable estimation of the burden of adverse neurobehavioral development attributable to PM_2.5 in pediatric populations and will inform local and global strategies for exposure prevention.

Background: Per- and polyfluoroalkyl substances (PFAS) are commonly utilized in consumer products. While earlier studies have suggested potential impacts of certain PFAS on serum concentrations of vitamin D, these investigations were constrained to a limited set of conventional PFAS. Moreover, they did not specifically focus on populations with longer duration of PFAS exposure and potentially higher blood PFAS levels, such as older adults, and lacked adequate evidence to examine sex-related disparities.

Methods: This observational investigation utilized cross-sectional data obtained from the U.S. NHANES spanning the years 2003 to 2018. Survey-weighted multiple regression models were employed to evaluate the relationship between PFAS exposure and vitamin D concentrations. Multi-pollutant models were employed to evaluate the association between PFAS mixtures and vitamin D concentrations. Subsequently, environmental risk scores (ERS) were constructed to gauge associations with vitamin D concentrations. ERS was computed through a weighted linear combination of PFAS, utilizing calculations from ridge regression and adaptive elasticity network (adENET) methodologies. All analyses were stratified by sex.

Results: The study encompassed 3,853 older adults. Our analysis revealed a negative association between PFOA, PFOS, PFNA, and MeFOSAA and serum vitamin D concentrations. In analyses examining mixed exposures, various models consistently indicated an inverse association between PFAS mixed exposure and vitamin D concentrations. Moreover, an increase in ERS of PFAS across the interquartile range was associated with a decrease in vitamin D concentrations (Q4 vs. Q1, adENET: β: -0.083, 95% CI: -0.117, -0.048; ridge regression: β: -0.077, 95% CI: -0.111, -0.042). Notably, these associations were exclusively observed within the female population.

Conclusions: Our study indicates that heightened exposure to PFAS correlates with diminished serum vitamin D concentrations in females aged 60 years and older, evident in both single and mixed exposures. These findings find support in in vitro mechanistic studies, suggesting that PFAS may impact the metabolism of 25(OH)D, consequently affecting vitamin D concentrations.

Epidemiologic research and quantitative risk assessment play a crucial role in transferring fundamental scientific knowledge to policymakers so they can take action to reduce the burden of ambient air pollution. This commentary addresses several challenges in quantitative risk assessment of air pollution that require close attention. The background to this discussion provides a summary of and conclusions from the epidemiological evidence on ambient air pollution and health outcomes accumulated since the 1990s. We focus on identifying relevant exposure-health outcome pairs, the associated concentration-response functions to be applied in a risk assessment, and several caveats in their application. We propose a structured and comprehensive framework for assessing the evidence levels associated with each exposure-health outcome pair within a health impact assessment context. Specific issues regarding the use of global or regional concentration-response functions, their shape, and the range of applicability are discussed.

Background: Substantial inequalities in the overall prevalence and patterns of multimorbidity have been widely reported, but the causal mechanisms are complex and not well understood. This study aimed to identify common patterns of multimorbidity in Serbia and assess their relationship with air pollutant concentrations and water quality indicators.

Methods: This ecological study was conducted on a nationally representative sample of the Serbian population. Data were obtained from the European Health Interview (EHIS) Survey, a periodic study designed to assess population health using widely recognized standardized instruments. The study included 13,069 participants aged 15 and older, randomly selected through a multistage stratified sampling design. Multimorbidity was defined as having two or more self-reported diagnoses of chronic non-communicable diseases. Latent class analysis (LCA) was performed to identify clusters of multimorbidity. Concentrations of particulate matter (PM10), sulfur dioxide (SO2), nitrogen dioxide (NO2), carbon monoxide (CO), and ozone (O3), as well as water quality indicators, were obtained from the Serbian Environmental Protection Agency.

Results: The overall prevalence of multimorbidity was 33.4% [32.6%-34.2%]. Six latent classes of multimorbidity were identified: Healthy, Multicondition, Cardiovascular, Metabolic syndrome, Respiratory, and Musculoskeletal. Annual increases in PM10 and SO2 concentrations, as well as daily increases in O3 concentrations, significantly raised the odds of having multimorbidity (OR = 1.02, 95% CI 1.02-1.03; OR = 1.01, 95% CI 1.00-1.02 and OR = 1.03, 95% CI 1.02-1.03, respectively). A pattern of increased risk was observed with rising levels of water contamination. Exposure to physico-chemical, microbiological and combined contamination was associated with a 3.92%, 5.17% and 5.54% higher probability, respectively, of having multiple chronic conditions. There was strong evidence that air pollutants, as well as chemical and microbial water contamination, were significantly associated with higher odds of the most common clusters of multimorbidity identified by LCA.

Conclusion: There is compelling evidence of an association between multimorbidity and environmental pollution, suggesting that exposure to air pollutants and water contaminants may contribute to disease accumulation and help explain geographically and socioeconomically patterned inequalities. These findings underscore the need for extensive studies that simultaneously measure both multimorbidity and pollution to explore their complex interrelationships.

Background: Whether including additional environmental risk factors improves cardiovascular disease (CVD) prediction is unclear. We attempted to improve CVD mortality prediction performance beyond traditional CVD risk factors by additionally using metals measured in the urine and blood and with statistical machine learning methods.

Methods: Our sample included 7,085 U.S. adults aged 40 years or older from the National Health and Nutrition Examination Survey 2003-2004 through 2015-2016, linked with the National Death Index through December 31, 2019. Data were randomly split into a 50/50 training dataset used to construct CVD mortality prediction models (n = 3542) and testing dataset used as validation to assess prediction performance (n = 3543). Relative to the traditional risk factors (age, sex, race/ethnicity, smoking status, systolic blood pressure, total and high-density lipoprotein cholesterol, hypertension, and diabetes), we compared models with an additional 17 blood and urinary metal concentrations. To build the prediction models, we used Cox proportional hazards, elastic-net (ENET) penalized Cox, and random survival forest methods.

Results: 420 participants died from CVD with 8.8 mean years of follow-up. Blood lead, cadmium, and mercury were associated (p < 0.005) with CVD mortality. Including these blood metals in a Cox model, initially containing only traditional risk factors, raised the C-index from 0.845 to 0.847. Additionally, the Net Reclassification Index showed that 23% of participants received a more accurate risk prediction. Further inclusion of urinary metals improved risk reclassification but not risk discrimination.

Conclusions: Incorporating blood metals slightly improved CVD mortality risk discrimination, while blood and urinary metals enhanced risk reclassification, highlighting their potential utility in improving cardiovascular risk assessments.

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.

Background: A large body of data shows that fetal brain development is vulnerable to disruption by air pollution experienced by the mother during pregnancy, adversely affecting cognitive and psychomotor capabilities during childhood (De Asis-Cruz et al., Biol Psychiatry 7:480-90, 2022; Morgan ZEM et al., Environ Health 22:11, 2023). This study has sought to identify gestational windows of susceptibility to prenatal exposure to air pollution.

Methods: 470 African American and Latina mother/child pairs participated in a prospective cohort study based in the low-income communities of Northern Manhattan and the South Bronx, New York City. Gestational exposure to respirable particulate matter (PM_2.5) and nitrogen dioxide (NO₂) was assessed through validated models in relation to cognitive and motor development assessed at ages 1, 2, and 3 years using the Bayley-II Scales. Multiple linear regression models and distributed lag models (DLM) were used to identify critical windows of exposure by trimester and week of pregnancy.

Results: By linear regression, average exposures to NO₂ during the first and second trimesters and the entire pregnancy were significantly and negatively associated with the mental developmental index (MDI) at age 1. Average exposures to PM_2.5 during the second trimester and the entire pregnancy were also significantly, inversely associated with age 1 MDI. No significant associations were found between these exposures and MDI at age 2. NO₂ exposure during the first trimester was significantly negatively associated with MDI at age 3. Using DLM, exposures to NO₂ at lags 29-30 weeks (within the first trimester) and PM_2.5 at lags 17-18 weeks (second trimester) were significantly and inversely associated with MDI at age 1. Significant, inverse associations were found between exposures to NO₂ at lag 29 weeks and PM_2.5 at lags 27-29 weeks and children's MDI at age 3. No significant associations were found between psychomotor index (PDI) and prenatal exposures to NO₂ or PM_2.5 at ages 1, 2 or 3.

Conclusions: Our finding that prenatal exposure to air pollution in the first and second trimesters was associated with lower scores for cognitive development at ages 1 and 3 is of concern because of the potential consequences of these outcomes for long-term functioning. They underscore the need for stronger policies to protect pregnant individuals and offspring, particularly during vulnerable, early life-stage of development.