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Environment International (EI) covers the broad field of environmental research that quantifies relationships between exposure to environmental contaminants and their relationship with environmental health. We recognize that environmental issues in relation to environmental health are truly interdisciplinary and therefore will consider articles that cover the entire spectrum of interactions, pathways, fate and effects for any chosen environmental hazard, either chemical, biological or physical. The primary criteria for publication are scientific quality and environmental health significance. Environmental epidemiology and biomarker-based risk assessment represent key areas which require integrated multidisciplinary research to identify, address and resolve current environmental health risk issues. We therefore encourage the submission of articles related to the identification and characterization of biological markers or 'biomarkers'. Biomarkers of exposure to environmental hazards, of environmentally-induced disease and of genetic susceptibility, are in combination revolutionizing the science of risk assessment. All of these measurements have the ability to improve the accuracy, reliability and scientific basis for the quantitative assessment of environmental health risks. We would welcome new approaches in these areas. Also, we particularly encourage papers concerned with issues relating to compounds that act as endocrine disrupters in the environment. This includes issues relating to mechanisms of action, testing, effects on wildlife and human exposure implications. No single format can accommodate all useful contributions to this journal. Five formats are offered: Editorial articles are published by our editor, members of the editorial board or invited guest editors. These focus attention on contemporary important environmental issues in relation to environmental health and are designed to stimulate debate and discussion. Research Articles are up-to-date original papers that present developments in any scientific field which relates environmental issues to health. Informative abstracts are required and articles must be fully referenced. Criteria for publication are weighted toward scientific quality and environmental significance. The manuscript will be evaluated on the basis of its conciseness, clarity, and presentation. The work will be assessed according to its originality, scientific merit, and experimental design. Poorly written manuscripts will be returned to the authors with a request to improve the quality of the paper prior to peer review. Reviews represent articles that emphasize recent developments in a particular field of research. They may be of a broader nature, providing summaries of new developments in any relevant area. Authors are encouraged to write in a clear and simple manner so that the article is unde
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The effect of exposure to radiofrequency fields on cancer risk in the general and working population: A systematic review of human observational studies - Part II: Less researched outcomes.
In the framework of the World Health Organization assessment of health effects of exposure to radiofrequency electromagnetic fields (RF-EMF), we have conducted a systematic review of human observational studies on the association between exposure to RF-EMF and risk of neoplastic diseases. Due to the extremely large number of included exposure types/settings and neoplasm combinations, we decided to present the review findings in two separate papers. In the first one we addressed the most investigated exposure-outcome pairs (e.g. glioma, meningioma, acoustic neuroma in relation to mobile phone use, or risk childhood leukemia in relation to environmental exposure from fixed-site transmitters) (Karipidis et al., 2024). Here, we report on less researched neoplasms, which include lymphohematopoietic system tumours, thyroid cancer and oral cavity/pharynx cancer, in relation to wireless phone use, or occupational RF exposure. Eligibility criteria: We included cohort and case-control studies of neoplasia risks in relation to three types of exposure to RF-EMF: 1. exposure from wireless phone use; 2. environmental exposure from fixed-site transmitters; 3. occupational exposures. In the current paper, we focus on less researched neoplasms including leukaemia, non-Hodgkin's lymphoma and thyroid cancer in mobile phone users; lymphohematopoietic system tumours and oral cavity/pharynx cancer in exposed workers. We focussed on investigations of specific neoplasms in relation to specific exposure sources (termed exposure-outcome pair, abbreviated E-O pairs), noting that a single article may address multiple E-O pairs. Eligible studies were identified by predefined literature searches through Medline, Embase, and EMF-Portal. Risk-of-bias (RoB) assessment: We used a tailored version of the Office of Health Assessment and Translation (OHAT) RoB tool to evaluate each study's internal validity. Then, the studies were classified into three tiers according to their overall potential for bias (low, moderate and high) in selected, predefined and relevant bias domains. We synthesized the study results using random effects restricted maximum likelihood (REML) models. Evidence assessment: Confidence in evidence was assessed according to the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) approach. We included 26 articles, which were published between 1988 and 2019, with participants from 10 countries, reporting on 143 different E-O pairs, including 65 different types of neoplasms. Of these, 19 E-O pairs satisfied the criteria for inclusion in quantitative syntheses of the evidence regarding the risks of leukaemia, non-Hodgkin's lymphoma or thyroid cancer in relation to mobile phone use, and the risks of lymphohematopoietic system tumours or oral cavity/pharynx cancer following occupational exposure to RF-EMF. RF-EMF exposure from mobile phones (ever or regular use vs no or non-regular use) was not associated with an increased risk of leukaemia [meta-estimate of the relative risk (mRR) = 0.99, 95 % CI 0.91-1.07, 4 studies), non-Hodgkin's lymphoma (mRR = 0.99, 95 % CI = 0.92-1.06, 5 studies), or thyroid cancer (mRR = 1.05, 95 % CI = 0.88-1.26, 3 studies). Long-term (10 + years) mobile phone use was also not associated with risk of leukaemia (mRR = 1.03, 95 % CI 0.85-1.24, 3 studies), non-Hodgkin lymphoma (mRR = 0.99, 95 % CI 0.86-1.15, 3 studies), or thyroid cancer (no pooled estimate given the small number of studies). There were not sufficient studies of any specific neoplasms to perform dose-response meta-analyses for either cumulative call time or cumulative number of calls; individual studies did not show statistically significant associations between lifetime intensity of mobile phone use and any specific neoplasm. Occupational RF-EMF exposure (exposed vs unexposed) was not associated with an increased risk of lymphohematopoietic system tumours (mRR = 1.03, 95 % CI = 0.87-1.28, 4 studies) or oral cavity/pharynx cancer (mRR = 0.68, 95 % CI 0.42-1.11, 3 studies). There were not sufficient studies of any specific neoplasms to perform meta-analysis on the intensity or duration of occupational RF-EMF exposure; individual studies did not show statistically significant associations with either of those exposure metrics and any specific neoplasms. The small number of studies, and of exposed cases in some instances, hampered the assessment of the statistical heterogeneity in findings across studies in the meta-analyses. Based on the summary risk of bias, most studies included in the quantitative evidence syntheses were classified at moderate risk of bias. The most critical issue was exposure information bias, especially for occupational studies where the exposure characterization was rated at high risk of bias for all included studies. Outcome information bias was an issue in mortality-based occupational cohort studies investigating non-rapidly fatal neoplasms. Further, the healthy subscriber effect, and (at a lesser extent) the healthy worker effect, were identified as plausible explanations of the decreased risks observed in some studies. The association of RF-EMF exposure from wireless phone use, or workplace equipment/devices, with other important neoplasms was reported by only one or two studies per tumour, so no quantitative evidence syntheses were conducted on these outcomes. It is noted that there were generally no statistically significant exposure-outcome associations for any combinations, independently of the exposure metric and level, with a few studies reporting decreased risks (especially for smoking-related cancers). There was only one study which assessed the effect of RF-EMF exposure from fixed-site transmitters on less researched neoplasms and it reported no statistically significant associations between exposure from base stations and risk of lymphomas overall, lymphoma subtypes, or chronic lymphatic leukaemia in adults. For near field RF-EMF exposure to the head from mobile phones, there was low certainty of evidence that it does not increase the risk of leukaemia, non-Hodgkin's lymphoma or thyroid cancer. For occupational RF-EMF exposure, there was very low certainty of evidence that it does not increase the risk of lymphohematopoietic system tumours or oral cavity/pharynx cancer. There was not sufficient evidence to assess the effect of whole-body far-field RF-EMF exposure from fixed-site transmitters (broadcasting antennas or base stations), or the effect of RF-EMF from any source on any other important neoplasms. This project was commissioned and partially funded by the World Health Organization (WHO). Co-financing was provided by the New Zealand Ministry of Health; the Istituto Superiore di Sanità in its capacity as a WHO Collaborating Centre for Radiation and Health; and ARPANSA as a WHO Collaborating Centre for Radiation Protection. PROSPERO CRD42021236798. Published protocol: [(Lagorio et al., 2021) DOI https://doi.org/10.1016/j.envint.2021.106828].
被引量：- 发表：1970
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Polystyrene nanoplastics promote colitis-associated cancer by disrupting lipid metabolism and inducing DNA damage.
Nanoplastics (NPs) have attracted widespread attention owing to their presence in the body. Recent studies highlighted the detrimental effects of NPs on the digestive tract. However, no studies have reported an association between NPs exposure and colitis-associated cancer (CAC). An azoxymethane/dextran sodium sulfate-induced CAC model was used, and polystyrene nanoparticles (PS-NPs) were selected for long-term exposure. Non-targeted metabolomics and 16S rRNA sequencing were used to detect changes in colonic metabolites and gut microbes following PS-NPs exposure. A lipopolysaccharide (LPS)-treated cancer cell model (Caco-2) exposed to PS-NPs was used to investigate the underlying molecular mechanism. Compared to the normal control group, mice in the PS-NPs group exhibited more tumor nodes and reactive oxygen species (ROS), higher expression of pan-CK and Ki-67, and more severe DNA damage. 16S rRNA sequencing revealed that exposure to PS-NPs altered the abundance of Allobaculum and Lactobacillus, whereas metabolic analysis showed that the most significant metabolites were enriched mostly in fatty acid metabolism. Experiments in LPS intervened Caco-2 cells showed that exposure to PS-NPs led to lipid peroxidation, oxidative stress, and DNA damage in Caco-2. Exposure to PS-NPs activated the phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway both in the AOM/DSS mouse model and cellular model. Key proteins involved in fatty acid metabolism were downregulated in Caco-2 cells exposed to PS-NPs. The metabolic effects of cancer cells exposed to PS-NPs were significantly inhibited by the activation of the fatty acid metabolism pathway by fenofibrate. PS-NPs exposure disturbed lipid metabolism and induced DNA damage via the activation of PI3K/AKT/mTOR to promote CAC progression. Inhibition of fatty acid metabolism is a therapeutic target for controlling PS-NP-induced CAC. Our study provides an important reference for the prevention and treatment of CAC from the perspective of the environment and enhances awareness of the necessity of plastic control.
被引量：- 发表：1970
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Understanding prenatal household exposures to per- and polyfluorylalkyl substances using paired Biological and dust measurements with sociodemographic and housing variables.
Per- and poly-fluoroalkyl substances (PFAS) are chemicals of concern-they are ubiquitous, persistent, with known and suspected health impacts. Well studied, primary sources of exposure to PFAS are drinking water and food. The presence of PFAS in human tissue of general populations suggests other important exposure sources/pathways. House dust measurements suggest widespread presence of PFAS in residences. Limited studies report paired analyses of PFAS occurrence in indoor media and PFAS concentrations in serum. While paired samples of house dust and blood serum are currently rare, the National Children's Study (NCS) contains paired samples, as well as sociodemographic information, from pregnant people that participated in the study. These archived NCS data and specimens for 104 participants collected between 2009 and 2014 were leveraged and analyzed for 16 commonly measured PFAS. We evaluated PFAS levels in the home, and the relationships between PFAS in dust and serum, and sociodemographic or housing variables. In addition, mechanistic exposure models, and then steady-state serum level models with simple parameters were used to estimate dust contributions of PFAS to serum. The geometric means for the most commonly found PFAS (full names in table 1) in serum were: 4.1 ng/mL for PFOS, 1.1 ng/mL for PFOA, 0.87 ng/mL for PFHxS, 0.16 ng/mL for PFDA. The geometric means of PFAS in dust were: 17 µg/kg for PFOS, 16 µg/kg for PFOA, 9.6 µg/kg for PFDS, 4.5 µg/kg for PFHpA, 4.4 µg/kg for PFNA, 3.9 µg/kg for PFHxS, 3.5 µg/kg for PFDA, 2.3 µg/kg for PFDoA, 2.1 µg/kg for PFUdA. PFOA was significantly correlated in serum and dust as was the sum of all PFAS detected in > 50 % of serum and dust. PFAS in serum was significantly associated with: Higher income, recent renovations, years lived in the home, and educational attainment. PFAS in dust was significantly associated with: Higher participant age, type of home, amount of carpet, educational attainment, higher income, recent renovation, and membership in the military. For some PFAS, 25 % of the overall exposure, on average, is from dust, but for others, 3-4 % is attributed to dust. We were able to identify important associations in PFAS exposure in the homes of pregnant people based on paired serum and dust samples. This built a clearer picture of which PFAS and at what quantities they exist in these homes, how they relate to each other, and how they are tied to sociodemographic and housing factors. Our results demonstrate that exposure to PFAS via house dust may contribute up to 25% of total exposure for adults, highlighting the importance of understanding what drives residential exposures.
被引量：- 发表：1970
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The effects of radiofrequency electromagnetic field exposure on biomarkers of oxidative stress in vivo and in vitro: A systematic review of experimental studies.
Oxidative stress is thought to be related to many diseases. Furthermore, it is hypothesized that radiofrequency electromagnetic fields (RF-EMF) may induce excessive oxidative stress in various cell types and thereby have the potential to compromise human and animal health. The objective of this systematic review (SR) is to summarize and evaluate the literature on the relation between the exposure to RF-EMF in the frequency range from 100 kHz to 300 GHz and biomarkers of oxidative stress. The SR framework was developed following the guidelines established in the WHO Handbook for Guideline Development and NTP/OHAT's Handbook for Conducting a Literature-Based Health Assessment. We used the latter handbook's methodology for implementing the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach for environmental health assessments. We searched the following databases up until June 30, 2023: PubMed, Embase, Web of Science Core Collection, Scopus, and the EMF-Portal. The reference lists of included studies and retrieved review articles were also manually searched. We rated Risk of Bias (RoB) using the OHAT RoB Rating Tool and assessed publication bias using funnel plots of included studies. We assessed the certainty of the evidence (high, moderate, low, or very low) for an association between RF-EMF and oxidative stress using an adapted version of the GRADE framework. Data were extracted according to a predefined set of forms developed in DistillerSR. Data were analysed after grouping them first as in vitro or in vivo and then according to outcome category, species category, and exposed tissue. We synthesized study results using a random effects meta-analysis when study characteristics were judged sufficiently similar to be combined and heterogeneity (I2) was lower than 75 %, otherwise we describe the findings narratively. Fifty-six (56) studies, 45 in vivo and 11 in vitro, in which cells (in vitro) or animals (in vivo) were exposed to frequencies in the range 800-2450 MHz, were included in the systematic review after eliminating 12,353 publications because they did not meet the criteria defined in the published protocol (Henschenmacher et al., 2022). Of 56 studies 52 studies with 169 individual results were included in the meta-analysis. Together, these studies examined six human in vitro samples and fifty animal samples, including rodents (mice, rats, hamsters, and guinea pigs, (n = 46)) and rabbits (n = 4). RF-EMF were predominantly applied as continuous wave exposures in these studies. The outcome biomarkers for modified proteins and amino acids were measured in n = 30 studies, for oxidized DNA bases in n = 26 studies, for oxidized lipids in n = 3 studies and hydrogen peroxide production in 2 studies. Outcomes were mostly measured in the brain (n = 22), liver (n = 9), cells (n = 9), blood (n = 6), and testis (n = 2). RoB in studies was high, mainly due to biases in exposure and outcome assessment. Brain: The effect on biomarkers for oxidized DNA bases in the rodent brain (five studies, n = 98) had an inconsistent effect, varying from a large decrease with a standardized mean difference (SMD) of -3.40 (95 % CI [-5.15, -1.64]) to a large increase with an SMD of 2.2 (95 % CI [0.78, 3.62]). In the brain of rabbits (two studies, n = 44), the effect sizes also varied, from an SMD of -1.06 (95 % CI [-2.13, 0.00]) to an SMD of 5.94 (95 % CI [3.14, 8.73]). The effect on biomarkers for modified proteins and amino acids in the rodent brain (15 studies, n = 328) also varied from a large decrease with an SMD of -6.11 (95 % CI [-8.16, -4.06]) to a large increase with an SMD of 5.33 (95 % CI [2.49, 8.17]). The effect on biomarkers for oxidized lipids in the brain of rodents (one study, n = 56) also varied from a large decrease with SMD = -4.10 (95 % CI [-5.48, -2.73]) to SMD = 1.27 (95 % CI [0.45, 2.10]). Liver: The effect on biomarkers for oxidized DNA bases in the rodent liver (two studies, n = 26) was inconsistent with effect sizes in both directions: SMD = -0.71 (95 % CI [-1.80, 0.38]) and SMD = 1.56 (95 % CI [0.19, 2.92]). The effect on biomarkers for oxidized DNA bases in the rabbits' liver (two studies, n = 60) was medium with a pooled SMD of 0.39 (95 % CI [-0.79, 1.56]). Biomarkers for modified proteins and amino acids in the liver of rodents (six studies, n = 159) increased with a pooled SMD of 0.55 (95 % CI [0.06, 1.05]). Blood: The effect of RF-EMF on biomarkers for oxidized DNA bases in rodent blood (four studies, n = 104) was inconsistent, with SMDs ranging from -1.14 (95 % CI [-2.23, -0.06]) to 1.71 (95 % CI [-0.10, 3.53]). RF-EMF had no effect on biomarkers for modified proteins and amino acids in rodent blood (three studies, n = 40), with a pooled SMD of -0.08 (95 % CI [-1.32, 1.16]). There was a large increase in biomarkers for oxidized DNA bases in rodent plasma (two studies, n = 38) with a pooled SMD of 2.25 (95 % CI [1.27, 3.24]). Gonads: There was an increase in biomarkers for oxidized DNA bases in the rodent testis (two studies, n = 24) with a pooled SMD of 1.60 (95 % CI [0.62, 2.59]). The effect of RF-EMF on biomarkers for modified proteins and amino acids in the ovary of rodents (two studies, n = 52) was inconsistent with a medium effect, SMD = 0.24 (95 % CI [-0.74, 1.23])) and a large effect (SMD = 2.08 (95 % CI [1.22, 2.94])). Thymus: RF-EMF increased biomarkers for modified proteins and amino acids in the thymus of rodents (one study, n = 42) considerably with a pooled SMD of 6.16 (95 % CI [3.55, 8.76]). Cells: RF-EMF increased oxidized DNA bases in rodent cells with SMD of 2.49 (95 % CI [1.30, 3.67]) (one study, n = 27). There was a medium effect in oxidized lipids (one study, n = 18) but not statistically significant with SMD = 0.34 (95 % CI [-0.62, 1.29]). In in vitro studies in human cells (three studies, n = 110), there were inconsistent increases in biomarkers for oxidized DNA bases, where the SMDs varied between 0.01 (95 % CI [-0.59, 0.62]) and 7.12 (95% CI [0.06, 14.18]) in 4 results (2 of them statistically significant). In rodent cells (three studies, n = 24), there was a not statistically significant large effect in biomarkers for oxidized DNA bases with SMD = 2.07 (95 % CI [-1.38, 5.52]). The RF-EMF biomarkers for modified proteins and amino acids in human cells (one study, n = 18) showed a large effect with SMD = 1.07 (95 % CI [-0.05, 2.19]). In rodent cells (two studies, n = 24) a medium effect of SMD = 0.56 (95 % CI [-0.29, 1.41]) was observed. The evidence on the relation between the exposure to RF-EMF and biomarkers of oxidative stress was of very low certainty, because a majority of the included studies were rated with a high RoB level and provided high heterogeneity. This is due to inaccurate measurements of exposure and/or of measurement of oxidative stress biomarkers and missing information on the blinding of research personnel to exposure conditions or outcome measurements. There may be no or an inconsistent effect of RF-EMF on biomarkers of oxidative stress in the brain, liver, blood, plasma and serum, and in the female reproductive system in animal experiments but the evidence is of very low certainty. There may be an increase in biomarkers of oxidative stress in testes, serum and thymus of rodents but the evidence is of very low certainty. Future studies should improve experimental designs and characterization of exposure systems as well as the use of validated biomarker measurements with positive controls. Other: This review was partially funded by the World Health Organization. The protocol for this review is registered in PROSPERO (https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42021235573) and published in Environment International (https://doi.org/10.1016/j.envint.2021.106932) (Henschenmacher et al., 2022).
被引量：- 发表：1970
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Prenatal exposure to per- and polyfluoroalkyl substances (PFAS) and their influence on inflammatory biomarkers in pregnancy: Findings from the LIFECODES cohort.
Per- and polyfluoroalkyl substances (PFAS) are fluorinated chemicals linked to adverse pregnancy and birth outcomes. However, the underlying mechanisms, specifically their effects on maternal inflammatory processes, are not well characterized. We examined associations between prenatal PFAS exposure and repeated measures of inflammatory biomarkers, including C-reactive protein (CRP) and four cytokines [Interleukin-10 (IL-10), IL-1β, IL-6, and tumor necrosis factor-α (TNF-α)]. We analyzed data from 469 pregnant women in a nested case-control study of preterm birth at Brigham and Women's Hospital in Boston, Massachusetts (2006-2008). We measured nine PFAS in early pregnancy plasma samples (median gestation: 10 weeks), with inflammatory biomarkers measured at median gestations of 10, 18, 26, and 35 weeks. We used linear mixed models for repeated measures and multivariable regression for visit-specific analysis to examine associations between each PFAS and inflammation biomarker, adjusting for maternal demographics, pre-pregnancy BMI, and parity. We examined the effects of PFAS mixture using sum of all PFAS (∑PFAS) and quantile-based g-computation approaches. We observed consistent inverse associations between most PFAS and cytokines, specifically IL-10, IL-6, and TNF-α, in both single pollutant and mixture analyses. For example, an interquartile range increase in perfluorooctanesulfonic acid was associated with -10.87 (95% CI: -19.75, -0.99), -13.91 (95% CI: -24.11, -2.34), and -8.63 (95% CI: -14.51, -2.35) percent change in IL-10, IL-6, and TNF-α levels, respectively. Fetal sex, maternal race, and visit-specific analyses showed associations between most PFAS and cytokines were generally stronger in mid-pregnancy and among women who delivered males or identified as African American. The observed suppression of both regulatory (IL-10) and pro-inflammatory (TNF-α) cytokines suggests that PFAS may alter maternal inflammatory processes or immune functions during pregnancy. Further research is needed to understand the effects of both legacy and newer PFAS on inflammatory pathways and their broader clinical implications.
被引量：- 发表：1970
