Environmental Health最新文献

Background: The detection of a local per- and polyfluoroalkyl substances (PFAS) pollution hotspot in Zwijndrecht (Belgium) necessitated immediate action to address health concerns of the local community. Several human biomonitoring (HBM) studies were initiated, gathering cross-sectional exposure data from more than 10,000 participants. The linkage of these HBM data with primary care health registries might be a useful new tool in environmental health analysis.

Aim: We assessed the feasibility of linking exposure data from HBM programs to health outcomes from the Intego registry, which collects data from general practitioners' electronic health records. This feasibility study uses exposure data from one of the completed PFAS HBM studies, which included 796 individuals. We describe the separate datasets, the process of integrating the HBM data into Intego, the analysis plan and the advantages and challenges of using this method.

Results: We established the integration of HBM data into the Intego primary care morbidity database, adhering to stringent privacy regulations and quality standards to ensure result integrity. Because of the modest sample size used in this feasibility study, no conclusions about the impact of PFAS on health endpoints can be drawn. However, with PFAS data from more than 10,000 residents available soon, more robust studies will be possible with this new method.

Interpretation: We introduce a novel approach for assessing the impact of environmental health hazards within primary care settings. The methods outlined here not only pave the way for larger-scale projects but also offer a promising avenue for long-term environmental health monitoring.

Background: Ambient air pollution is a known risk factor for several chronic health conditions, including pulmonary dysfunction. In recent years, studies have shown a positive association between exposure to air pollutants and the incidence, morbidity, and mortality of a COVID-19 infection, however the time period for which air pollution exposure is most relevant for the COVID-19 outcome is still not defined. The aim of this study was to analyze the difference in association when varying the time period of air pollution exposure considered on COVID-19 infection within the same cohort during the first wave of the pandemic in 2020.

Methods: We conducted a cross-sectional study analyzing the association between long- (10- and 2-years) and short-term (28 days, 7 days, and 2 days) exposure to NO₂ and PM_2.5 on SARS-CoV-2 incidence, morbidity, and mortality at the level of county during the first outbreak of the pandemic in spring 2020. Health data were extracted from the German national public health institute (Robert-Koch-Institute) and from the German Interdisciplinary Association for Intensive Care and Emergency Medicine. Air pollution data were taken from the APExpose dataset (version 2.0). We used negative binomial models, including adjustment for risk factors (age, sex, days since first COVID-19 case, population density, socio-economic and health parameters).

Results: We found that PM_2.5 and NO₂ exposure 28 days before COVID-19 infection had the highest association with infection, morbidity as well as mortality, as compared to long-term or short-term (2 or 7 days) air pollutant exposure. A 1 μg/m³ increase in PM_2.5 was associated with a 31.7% increase in incidence, a 20.6% need for ICU treatment, a 23.1% need for mechanical ventilation, and a 55.3% increase in mortality; an increase of 1 μg/m³ of NO₂ was associated with an increase for all outcomes by 25.2 - 29.4%.

Conclusions: Our findings show a positive association between PM_2.5 and NO₂ exposure and the clinical course of a SARS-CoV2 infection, with the strongest association to 28 days of exposure to air pollution. This finding provides an indication as to the primary underlying pathophysiology, and can therefore help to improve the resilience of societies by implementing adequate measures to reduce the air pollutant impact on health outcomes.

Trial registration: Not applicable.

Background: Congenital heart disease (CHD) is a common birth defect. Our previous studies suggest that indoor air pollution, especially total volatile organic compounds (TVOCs), may increase fetal CHD risk, whereas vitamin and folic acid (FA) supplements in early pregnancy might offer protection against CHD. However, limited research has explored whether FA or multivitamin supplementation can mitigate the effects of TVOCs exposure on CHD.

Methods: We conducted a case-control study to investigate the association between maternal nutrient supplementation, household indoor air pollutant exposure during pregnancy, and CHD in offspring. Pregnant women with 22-30 gestational weeks were recruited from two hospitals in East China between January 2016 and March 2022. A comprehensive approach was used, incorporating questionnaires to collect nutrient supplement information, blood sample analysis to detect serum folate, vitamin B12, and homocysteine (HCY) concentrations, and field investigations to assess indoor benzene, toluene, xylene, formaldehyde, and TVOCs exposures. Logistic regression analysis was performed to identify CHD risk factors, and stratified analysis was used to evaluate the combined effects of nutrient supplementation and TVOCs on CHD.

Results: The study included 53 cases and 77 controls. Logistic regression analysis identified high maternal serum HCY (> 6.125 µmol/L) and high household TVOCs exposure (> 0.0165 mg/m³) as risk factors for CHD in offspring, with adjusted odds ratios of 2.98 (95% CI: 1.31-6.36) and 9.23 (95% CI: 3.78-22.53), respectively. Regular multivitamin supplementation mitigated the risk of high TVOCs exposure on fetal CHD, while the adverse effect of high serum HCY-related CHD risk was attenuated in the group with regular FA supplementation.

Conclusion: Exposure to high indoor TVOCs concentrations increases the risk of fetal CHD. Regular multivitamin supplementation may reduce the adverse effects of high TVOCs exposure on fetal CHD.

Background: Long-term air pollution exposure and inflammation are considered to be associated with cognitive decline. However, whether air pollution exposure related cognitive decline is dependent on inflammation remains uncertain.

Materials and methods: The present study collected data from China Health and Retirement Longitudinal Study (CHARLS) at baseline in 2011, with a follow up period in 2015. Concentration of air pollutants (particles with diameters ≤ 1.0 μm [PM₁], ≤ 2.5 μm [PM_2.5], ≤ 10 μm [PM₁₀], nitrogen dioxide [NO₂] and ozone [O₃]) were obtained from China High Air Pollutants (CHAP) dataset. Hypersensitive C-reactive protein (hs-CRP), a systemic inflammation marker, was measured in blood of subjects and cognitive function was assessed by standardized questionnaire.

Results: A total of 6434 participants were included in the study. Lower exposure to PM_2.5, PM₁, PM₁₀ and NO₂ were associated with mitigated cognitive decline. The odds ratios (ORs) for air pollutants changes and cognitive decline and 95% confidence intervals (CIs) were as follows: PM_2.5-0.934(0.925, 0.943), PM₁- 0.945 (0.935,0.955), PM₁₀-0.977(0.972,0.982) and NO₂-0.962(0.950,0.975), respectively. Hs-CRP showed no significant correlation with cognitive decline or change in levels of air pollution. The interaction regression analyses, both unadjusted and adjusted, did not uncover any significant correlation between hs-CRP and air pollution with respect to cognitive decline. Bootstrap test exhibited no significant mediating effect of hs-CRP on the relationship between any air pollutants and cognitive decline, the indirect effects of hs-CRP in conjunction with exposure to different air pollutants were all found to be non-significant, with the following bootstrap CIs and p-values: PM_2.5-1.000([1.000,1.000], P = 0.480),PM₁-1.000([1.000,1.000], P = 0.230),PM₁₀-1.000([1.000,1.000], P = 0.650), O₃-1.000([1.000,1.000], P = 0.470), ΔNO₂-1.000([1.000,1.000], P = 0.830) .

Conclusion: Ambient air pollution exposure was linked to cognitive decline independent of hs-CRP level.

Background: Existing evidence for associations of per- and polyfluoroalkyl substances (PFASs) with blood lipids, lipoproteins and apolipoproteins (apo), and coronary heart disease (CHD) risk is limited and inconsistent. This study aims to explore associations between plasma PFASs, blood lipoprotein subspecies defined by apolipoproteins, and CHD risk.

Methods: A case-control study of CHD was conducted in the Health Professionals Follow-Up Study (HPFS) and Nurses' Health Study (NHS). Among participants initially free of cardiovascular disease at blood collection in 1994 (HPFS) or 1990 (NHS), 101 participants who developed non-fatal myocardial infarction or fatal CHD were identified and confirmed. A healthy control was matched to each case for age, smoking status, and date of blood draw. Plasma levels of perfluorohexane sulfonic acid (PFHxS), perfluorooctanoic acid (PFOA), total perfluorooctane sulfonic acid (PFOS), branched PFOS (brPFOS), linear PFOS (nPFOS), perfluorononanoic acid (PFNA), and perfluorodecanoic acid (PFDA) were measured. Conditional logistic regression and cubic spline regression models were used to examine associations between baseline PFASs and CHD risk. Linear regression models were applied to study PFAS associations with lipids and their subfractions.

Results: After multivariate adjustments, total PFOS, brPFOS and nPFOS were significantly associated with increased risk of developing CHD, and HRs (95% CIs) per log(ng/mL) increment of PFASs were 3.66 (1.36-9.89), 3.68 (1.55-8.76), and 3.01 (1.16-7.86), respectively. Significant positive dose-response relationships were identified for these PFASs (P_linearity = 0.01, 0.002, 0.02, respectively). Other PFASs were not associated with CHD risk. PFNA and PFDA were positively associated with total apoE levels among HDL particles with or without apoC-III. No associations were observed for other PFASs with blood lipid subspecies. Blood lipid subfractions did not explain the association between PFOS and CHD risk.

Conclusions: Plasma PFOS and its isomers were positively associated with CHD risk. These findings suggest that PFOS exposure causes public health risks that are greater than hitherto believed.

Introduction: Ionizing radiation is a human carcinogen, and there is a public concern but limited evidence that it increases the incidence of cancer among those who live near nuclear power plants (NPPs). Previous analyses of thyroid cancer in these populations have been inconsistent, and the last synthesis was published nearly a decade ago. To address these gaps, we undertook a systematic review and meta-analysis.

Methods: A search strategy was developed and applied to PubMed, Scopus, and Web of Science databases. A total of 2006 publications were identified, with 11 studies of thyroid cancer incidence that met the inclusion criteria. Study quality was assessed using the Office of Health Assessment and Translation (OHAT) tool. Summary risk estimates relating residential proximity to the NPPs and thyroid cancer were generated using a random effects model. Heterogeneity in the risk estimates was assessed for study features that included: distance to the NPP, study quality, and biological sex.

Results: The 11 studies were categorized as either highly (n = 8) or plausibly (n = 3) prone to bias, primarily due to the reliance on ecological study designs. The meta-analysis summary relative risk of thyroid cancer among those who live close to NPPs (defined by ≤ 25 km distance or jurisdictional areas (e.g., community, county) relative to those who lived further away was 1.09 (95% CI: 0.93-1.29). The risk estimates were higher for studies that modelled more proximal residential distances (≤ 5 km) to NPPs than larger distances (≤ 25 km and jurisdictional areas). We found that the summary risk (RR=1.29, 95% CI: 0.77-2.16) was stronger among those studies less prone to bias. A non-significant increased risk was found among both men and women, but there was no evidence of sex differences in risk.

Conclusion: Overall, the findings suggest that living near a nuclear power plant increases the risk of thyroid cancer. The small number of studies on this topic, and the finding of higher risks in studies less prone to bias highlights the need for better-designed studies.

Background: Ambient air pollution is recognized as a major risk factor for chronic obstructive pulmonary disease (COPD) which is the third leading cause of death worldwide. We examined whether variations in daily outdoor air pollutants levels were associated with excess hospital emergency room visits (ERV) for acute exacerbation of COPD (AECOPD).

Methods: This two-center ecological cohort study was conducted in Amiens, France. We collected all consecutive ERV for AECOPD throughout 2017 and developed single pollutant models to assess the association between AECOPD and nitrogen dioxide (NO₂), ozone (O₃), or particulate matter (PM_2.5 and PM₁₀) levels, while adjusting for temperature, hygrometry, influenza circulation and pollen allergy risk. For a subgroup of patients, we also applied geographical modeling to analyze annual exposure to outdoor air pollutants.

Results: We recorded 240 ERV among 168 COPD patients in 2017 and identified 9 peaks of ERV. There was a statistically significant positive correlation between the daily ERV for AECOPD and the daily average concentrations of PM_2.5 (RR = 1.06 (95%CI = [1.00-1.11]), p = 0.049), but no correlation with NO₂, O₃ or PM₁₀ (p = 0.073, p = 0.114 and p = 0.119, respectively). Our geographical modeling study revealed that long-term exposure to any of the four outdoor air pollutants was not associated with more frequent AECOPD.

Conclusion: Even though the pollution levels measured generally remained below or near the 2021 short-term air quality guidelines issued by the World Health Organization, significant aggregate-level associations were found between severe AECOPD leading to ERV and daily concentrations of PM_2.5.

Clinical trial registration: NCT03079661.

Background: Perfluoroalkyl and polyfluoroalkyl substances (PFAS) exposure has been associated with metabolic diseases, however, the underlying molecular pathogenesis remains to be understood. Integrated PFAS and lipidomic analysis has the potential to identify alterations in lipid metabolism pathways for exposome research.

Methods: A targeted LC-MS/MS method was developed for the quantification of 14 PFAS from human plasma samples (n = 96). Concurrently, high coverage lipidomics was conducted for the quantification of 665 lipid species in the same plasma samples. Linear regression models were implemented to study the association of PFAS with plasma lipidome.

Results: Women had lower levels of PFAS compared to men and Asian-Indians had lower levels of PFAS compared to both Chinese and Malay subjects. PFAS were positively associated with a number of lipid species from lysophospholipid, ceramide and triacylglycerol lipid classes. Phosphatidylinositol, acylcarnitine and sphingosine-1-phosphate were negatively associated with PFAS. Association studies revealed both shared and distinct relationship of PFAS with plasma lipids.

Conclusions: We demonstrate that the circulating levels of PFAS vary with age, ethnicity and sex within a multi-ethnic Asian population with potential implications in future biomonitoring and mitigation. Our comprehensive lipidomics methodology and association studies enabled us to characterize the relationship of circulating PFAS and lipidomic profiles. These results will help in better understanding of the molecular basis of PFAS exposure on human health outcomes.

Background: Previous studies on the associations of per- and polyfluoroalkyl substances (PFASs) and heavy metals with lipid profiles among adolescents have been scarce. We sought to investigate the associations of PFASs and heavy metals with blood lipid levels in a representative sample of Korean adolescents.

Methods: Data from the Korean National Environmental Health Survey (2018-2020) were used. Concentrations of PFASs [perfluorooctanoic acid (PFOA), perfluorooctane sulfonic acid (PFOS), perfluorohexane sulfonic acid, perfluorononanoic acid (PFNA), and perfluorodecanoic acid (PFDeA)], lead, and mercury were measured in serum, whole blood, and urine samples, respectively. Linear regression, Bayesian kernel machine regression (BKMR), and k-means clustering analyses were employed to evaluate the associations between pollutants and lipid levels.

Results: In the linear regression analyses, PFOA levels were associated with higher low-density lipoprotein cholesterol (LDL-C) levels; PFOS with higher total cholesterol (TC) levels; PFNA with higher TC, LDL-C, and non-high-density lipoprotein cholesterol (non-HDL-C) levels; PFDeA with higher TC, LDL-C, non-HDL-C, and high-density lipoprotein cholesterol levels; and mercury with higher TC and non-HDL-C levels. The BKMR analysis revealed that the PFAS and heavy metal mixture was associated with higher LDL-C levels (1.8% increase in LDL-C at the 75th percentile of all PFAS and heavy metal concentrations compared to their median values, 95% credible interval: 0.5, 3.1), primarily driven by the effect of PFDeA. Compared to individuals in the low pollutant exposure cluster (geometric mean levels of PFOA, PFOS, PFHxS, PFNA, PFDeA, lead, and mercury were 2.7 μg/L, 6.2 μg/L, 1.6 μg/L, 0.7 μg/L, 0.4 μg/L, 0.8 μg/dL, and 0.3 μg/L, respectively), those in the high pollutant exposure cluster (5.1 μg/L, 10.7 μg/L, 3.7 μg/L, 1.3 μg/L, 0.6 μg/L, 0.9 μg/dL, and 0.4 μg/L, respectively) demonstrated higher TC levels (2.5% increase in TC, 95% confidence interval: 0.1, 5.0) in the k-means clustering analysis.

Conclusion: Due to the limitations of this study, such as its cross-sectional design, these results should be interpreted cautiously and confirmed in future studies before drawing implications for public health strategies aimed at promoting health during adolescence and later in life.