Reviews on Environmental Health最新文献

Endocrine-disrupting chemicals are commonly found in food due to their migration from plastic packaging. Despite their functional benefits, these additives can disrupt the endocrine system, leading to several adverse health outcomes. This review aims to examine the migration of phthalates, bisphenols, and per-and-polyfluoroalkyl substances (PFAS) from plastic food packaging into food substances. Six electronic databases were systematically screened for observational, case reports, or experimental studies investigating any food for human consumption exposed to food packaging. Sixty-seven studies, including 5,378 samples, were included. Phthalates and bisphenols consistently migrated from food packaging. PFAS migration was also detected but too few studies were published to draw conclusions. Migration rates were influenced by factors such as temperature, exposure time, and food composition, with high-fat or acidic foods leading to higher migration rates. Based on a standard Western Diet, 713.8 µg of di-2-ethylhexyl phthalate, 347.7 µg of di-n-butyl phthalate, 17.3 µg of butyl-benzyl phthalate, 35,250 µg of di-iso-decyl phthalate, and 65.4 µg of other plasticizers, totaling 36,349.2 µg, could be consumed from food packaging daily. However, these estimates may not be generalizable to other dietary patterns, such as Mediterranean or plant-based diets. Further research into low migration or safer alternative to current plasticizers, alongside regulatory efforts considering potential exposure via food contact materials may help reduce risks associated with endocrine-disrupting chemicals in food packaging.

Millions of people worldwide are chronically exposed to environmental arsenic through drinking water, increasing their risk of various adverse cardiometabolic outcomes. To understand the inter-individual variation in arsenic susceptibility, this systematic review explores all epidemiological evidence on interactions between single nucleotide polymorphisms (SNPs) and arsenic exposure in relation to cardiometabolic health. Five electronic databases were searched until April 2023. From 42,202 retrieved publications, 18 candidate gene-environment (cGxE) studies were included, and no genome-wide association studies were found. Of 676 SNPs in 148 genes tested, 40 SNPs in 24 genes, 4 haplotypes and combined SNPs in MCP-1/APOE, were reported to statistically significantly interact with arsenic exposure. These genes were involved in arsenic metabolism, oxidative stress or defence, DNA damage repair, endothelial (dys) function, inflammation or immune function, tumour suppressor activity, or were previously implicated in cardiometabolic disease pathways. Most studies did not explore the same SNPs (or strong proxies), and none of the identified SNP-arsenic interactions were replicated for the same arsenic species and cardiometabolic outcome. Whilst some SNPs are suggestive of influencing susceptibility to arsenic for various cardiometabolic outcomes, further research is needed to understand the interplay between arsenic and genetic variants, identify at-risk populations, and improve risk assessment.

Studies examining the relationship between fine particulate matter (PM_2.5) exposure and cancer risk is inconclusive, with an evident scarcity of comprehensive data on the overall cancer risk. Given the emergence of new evidence, updated meta-analyses is essential. A search was performed on multiple databases including PubMed, Embase, Scopus, Web of Science, and the Cochrane Library up to Jan 2025. Hazard ratios (HRs), relative risks (RRs), or incidence rate ratios (IRRs) with their 95 % confidence intervals (CIs) were extracted and pooled. Moreover, a comprehensive and detailed quality assessment of the included studies was conducted to validate the plausibility of the findings. Overall, 57 original studies were included, covering 36 cancer categories and including overall cancer and malignancies specific to particular anatomical sites. For each increase of 10 μg per cubic meter in PM_2.5 concentration, there was an observed pooled HR of 1.07 for overall cancer (95 %CI:1.02-1.13). In the case of site-specific cancers, the pooled HRs were 1.11 (95 %CI:1.07-1.15), 1.06 (95 %CI:1.02-1.11), 1.17 (95 %CI:1.07-1.28), and 1.14 (95 %CI:1.03-1.26) for lung, breast, liver and esophageal cancers, respectively. Furthermore, PM_2.5 exposure may potentially correlate with the risk of cancers at other anatomical locations including upper aerodigestive tract, oral cavity, kidney, skin, as well as digestive organs. In light of available evidence, it is inferred that PM_2.5 exposure could potentially raise overall cancer risk with moderate certainty. As for site-specific malignancies, there is very low certainty evidence for lung cancer, low certainty evidence for breast cancer, and moderate certainty evidence for both liver and esophageal cancers.

Communities living in proximity to coal-fired power plants (CFPPs) may be at greater risk of negative health impacts from exposure to air pollution than communities living further away. The aim of this scoping review was to provide an update on the evidence of the health risks of air pollution exposure associated with living in proximity to CFPPs and to evaluate the relationship between residential proximity and the extent of the health burden. We followed the PRISMA-ScR guidelines and searched Google Scholar, PubMed, ScienceDirect, Scopus and Web of Science for relevant studies from inception up to 31 January 2024. Fifty-six studies were included with most articles published from 2016 to 2023 (n=33, 59 %) and 35 were in high income countries (63 %). Living close to CFPPs was frequently associated with increased odds or likelihood of respiratory disorders, adverse birth outcomes and child developmental issues. Interventions such as emission control systems or total shutdown of CFPPs led to improved health among communities living near CFPPs. The review highlights the health impacts from air pollution associated with living in proximity to CFPPs and the need for policy measures to reduce air pollution by installing emission control technologies or transitioning to cleaner energy sources.

Some studies have shown that maternal exposure to perfluoroalkyl substances (PFAS) may be related to the neonatal birth weight. The purpose of this study was to explore this relationship between maternal exposure to PFAS and neonatal birth weight. All papers published before March 2024 were retrieved from the Web of Science, PubMed, and Embase databases. A thorough meta-analysis was carried out, involving data extracted from 1,673 samples obtained from a total of 24 articles. Our study found a significantly negative association between maternal PFOS exposure and neonatal birth weight (β= -71.55; 95 %CI= -114.47, -28.62), with high heterogeneity (I ² =64.15 %, p<0.0001). Similarly, there was a significant negative correlation between maternal PFOA exposure and neonatal birth weight (β= -81.26; 95 %CI= -126.08, -36.43), with high heterogeneity (I ² =67.23 %, p<0.0001). Subunit analysis showed that there was a significantly negative correlation between PFOS exposure and neonatal birth weight in mid-to-late pregnancy and after delivery (β= -97.87; 95 %CI= -181.83, -13.92, β= -138.06; 95 %CI= -255.91, -20.20), PFOA exposure showed a negative correlation with neonatal birth weight in mid-to-late pregnancy (β= -85.89; 95 %CI= -139.31, -32.47), while PFNA exposure also showed a negative correlation with neonatal birth weight in mid-to-late pregnancy (β= -90.39; 95 %CI= -152.90, -27.88). However, no significant correlation was observed for PFNA exposure (β=3.95; 95% CI= -10.41, 18.31), with medium heterogeneity (I ² =40.56 %, p=0.0574), or for PFHxS exposure (β=4.61; 95 %CI= -10.60, 19.81), with medium heterogeneity (I ² =29.27 %, p=0.1368). Further research is needed to better understand the implications of these findings on maternal and neonatal health.

The question of whether dichlorodiphenyltrichloroethane (DDT) exposure is related to breast cancer (BC) remains unanswered, possibly due to methodological constraints in the studies that have been performed. We aimed to update and synthesize the available epidemiological evidence on the relationship of p,p'-DDT, o,p'-DDT and p,p'-dichlorodiphenyldichloroethylene (p,p'- DDE) biological concentrations with female BC, focusing in methodological characteristics not addressed in previous reviews. We conducted an overview of reviews and a systematic review and meta-analysis. We used six databases and one search engine to identify meta-analyses based on systematic reviews, pooled analyses, and individual studies published from January 2000 to December 2021. For the overview of reviews, we assessed meta-analyses' risk of bias and carried out a narrative synthesis. For the meta-analysis, we estimated summary association measures with fixed or random effects models for each compound stratifying for characteristics of interest. We estimated a positive summary association between p,p'- DDT biological concentrations and BC in prospective studies (nested case control) with >10 years of follow-up (sOR=1.41; 95 %CI: 1.06-1.88). Among retrospective studies (hospital or population-based case-control), BC was positively related with p,p'-DDE biological concentrations (sOR=1.15; 95 %CI: 1.02-1.30), and with p,p'-DDT in women with mean serum concentrations>100 ng/g (sOR=1.33; 95 %CI: 1.25-1.41). Moreover, we detected a positive association between o,p'-DDT and BC (sOR=2.24; 95 %CI: 2.15-2.34). Our results support a positive relationship between DDT exposure and BC, and are useful to reinforce its worldwide prohibition, since this pesticide is still used in some countries, has long persistence in the human body and disseminates to other geographic areas.

In several industrialized countries, there has been a report of a decrease in the proportion of male births. The current study is designed to perform a systematic review and present a comprehensive summary of current epidemiological evidence of an association between exposure to the mentioned pollutants and sex ratio. The present systematic review was executed according to the PRISMA protocol. A comprehensive online search was performed in PubMed Medline, Scopus, Web of Science, Embase databases, Google Scholar, and the World Health Organization databases from 2000 to September 2023. After searching all databases, 20 articles were included in this systematic review. Regarding the studied pollutants found that exposure to increased PM₁₀, PM_2.5, and Nitrogen dioxide (NO₂) levels was significantly associated with the sex ratio. Both maternal Benzophenone (BP)-2 and paternal BP-2 were significantly associated with an excess of female births. Finally, it must be said that the effect of some environmental pollutants on the sex ratio is undeniable. However, the sex ratio is the result of multiple factors that interact simultaneously during pregnancy. Additional research is required to examine the mechanisms responsible for the change in sex ratio.

Plastic waste enters the oceans and soil and is consumed by organisms and humans. Some of the ingested microplastics may remain in the human body and cause toxicity. We conducted a systematic review to estimate the extent to which humans are exposed to microplastics through consumption and performed a quality assessment of research results. We searched for studies published up to December 2023 and included studies that reported on the characteristics and estimated intake of microplastics. The quality assessment tool reported in previous studies was used for food and drinking water studies. We included 76 studies in the analysis, and the types of foods were classified into seven categories: seafood, drinking water, table salt, fruits and vegetables, beverages, condiments, and meat. The estimated daily intake of microplastics via food was 0.0002-1,531,524 MP/day, with the highest value in bottled water. The quality of food and drinking water studies was evaluated using a quantitative tool to assess reliability. The quality of food studies was 11.50 out of 20 points and the quality of drinking water studies was 11.16 out of 19 points. These results indicate that the closer the score is to the maximum, the more reliable the research findings. The quantitative assessment can be used as an indicator for evaluating the risks of microplastics and can help reduce biases that may occur during the research process. This study confirmed microplastics in foods and human exposure to up to one million microplastics daily. Our study emphasizes the potential for microplastic exposure through food intake and subsequent accumulation in the human body; therefore, efforts are needed to reduce exposure to microplastics in daily life.

The present review aimed to evaluate the apoptotic effect of tributyltin (TBT) exposure on mammalian tissues and cells in vivo. A search was conducted in specialized literature databases including Embase, Medline, Pubmed, Scholar Google, and Scopus for all manuscripts using the following keywords: "tributyltin", "apoptosis", "mammals", "mammalian cells', "eukaryotic cells", 'rodents', "rats", "mice" and "in vivo" for all data published until September 2023. A total of 16 studies were included. The studies have demonstrated that TBT exposure induces apoptosis in cells from various mammalian organs or tissues in vivo. TBT is capable to increase apoptotic cells, to activate proapoptotic proteins such as calpain, caspases, bax and beclin-1 and to inhibit antiapoptotic protein bcl-2. Additionally, TBT alters the ratio of bcl-2/bax which favor apoptosis. Therefore, the activation of enzymes such as calpain induces apoptosis mediated by ERS and caspases through the intrinsic apoptosis pathway. This review has demonstrated that TBT exposure induces apoptosis in mammalian tissues and cells in vivo.