Heavy metals are naturally occurring components of the Earth's crust and persistent environmental pollutants. Human exposure to heavy metals occurs via various pathways, including inhalation of air/dust particles, ingesting contaminated water or soil, or through the food chain. Their bioaccumulation may lead to diverse toxic effects affecting different body tissues and organ systems. The toxicity of heavy metals depends on the properties of the given metal, dose, route, duration of exposure (acute or chronic), and extent of bioaccumulation. The detrimental impacts of heavy metals on human health are largely linked to their capacity to interfere with antioxidant defense mechanisms, primarily through their interaction with intracellular glutathione (GSH) or sulfhydryl groups (R-SH) of antioxidant enzymes such as superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), glutathione reductase (GR), and other enzyme systems. Although arsenic (As) is believed to bind directly to critical thiols, alternative hydrogen peroxide production processes have also been postulated. Heavy metals are known to interfere with signaling pathways and affect a variety of cellular processes, including cell growth, proliferation, survival, metabolism, and apoptosis. For example, cadmium can affect the BLC-2 family of proteins involved in mitochondrial death via the overexpression of antiapoptotic Bcl-2 and the suppression of proapoptotic (BAX, BAK) mechanisms, thus increasing the resistance of various cells to undergo malignant transformation. Nuclear factor erythroid 2-related factor 2 (Nrf2) is an important regulator of antioxidant enzymes, the level of oxidative stress, and cellular resistance to oxidants and has been shown to act as a double-edged sword in response to arsenic-induced oxidative stress. Another mechanism of significant health threats and heavy metal (e.g., Pb) toxicity involves the substitution of essential metals (e.g., calcium (Ca), copper (Cu), and iron (Fe)) with structurally similar heavy metals (e.g., cadmium (Cd) and lead (Pb)) in the metal-binding sites of proteins. Displaced essential redox metals (copper, iron, manganese) from their natural metal-binding sites can catalyze the decomposition of hydrogen peroxide via the Fenton reaction and generate damaging ROS such as hydroxyl radicals, causing damage to lipids, proteins, and DNA. Conversely, some heavy metals, such as cadmium, can suppress the synthesis of nitric oxide radical (NO·), manifested by altered vasorelaxation and, consequently, blood pressure regulation. Pb-induced oxidative stress has been shown to be indirectly responsible for the depletion of nitric oxide due to its interaction with superoxide radical (O2·-), resulting in the formation of a potent biological oxidant, peroxynitrite (ONOO-). This review comprehensively discusses the mechanisms of heavy metal toxicity and their health effects. Aluminum (Al), cadmium (Cd), arsenic (As), mercury (Hg), lead (Pb), and chromium (Cr) and their roles in the development of gastrointestinal, pulmonary, kidney, reproductive, neurodegenerative (Alzheimer's and Parkinson's diseases), cardiovascular, and cancer (e.g. renal, lung, skin, stomach) diseases are discussed. A short account is devoted to the detoxification of heavy metals by chelation via the use of ethylenediaminetetraacetic acid (EDTA), dimercaprol (BAL), 2,3-dimercaptosuccinic acid (DMSA), 2,3-dimercapto-1-propane sulfonic acid (DMPS), and penicillamine chelators.

• Klíčová slova
• Antioxidant enzymes, Heavy metals, Human disease, Oxidative stress, ROS, Toxicity,
• MeSH
• antioxidancia metabolismus   MeSH
• bioakumulace MeSH
• látky znečišťující životní prostředí toxicita   MeSH
• lidé MeSH
• oxidační stres * účinky léků   MeSH
• těžké kovy * toxicita   MeSH
• vystavení vlivu životního prostředí škodlivé účinky   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• antioxidancia MeSH
• látky znečišťující životní prostředí MeSH
• těžké kovy * MeSH

OBJECTIVES: Polychlorinated biphenyls (PCBs), a family of persistent toxic and organic environmental pollutants, were associated with multiple organ damages in humans once accumulating. However, association between PCBs exposure and circulatory immune markers were not clear. METHODS: Data was collected from participants enrolled in the National Health and Nutrition Examination Survey in 1999-2004. PCBs were categorized by latent class analysis (LCA). Weighted quantile sum (WQS) regression was used to investigate effects of PCBs exposure on circulatory immune markers including leukocyte counts, monocyte-lymphocyte ratio (MLR), neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR), and systemic immune-inflammation index (SII). RESULTS: There were 3,109 participants included in the final analysis with blood PCBs levels presented as 3 classes. The high PCBs group had a higher rate of comorbidities. Leukocyte, lymphocyte and neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR) and system immune-inflammation index (SII) were significantly lower in the high PCBs group than in the low PCBs group (all p-values < 0.05). After adjusting for covariant variables, the low PCBs group was positively associated with SII (p = 0.021) and NLR (p = 0.006) in multivariate regression. Significantly negative correlations between PCBs classification and SII (β = -14.513, p = 0.047), and NLR (β = -0.035, p = 0.017) were found in WQS models. LBX028LA showed the most significant contribution in the associations between PCBs and SII, and LBX128LA contributed most significantly to associations with NLR. CONCLUSION: Our study adds novel evidence that exposures to PCBs may be adversely associated with the circulatory immune markers, indicating the potential toxic effect of PCBs on the human immune system.

• Klíčová slova
• circulatory immune markers, latent class analysis, platelet-lymphocyte ratio, polychlorinated biphenyls, systemic immune-inflammation index, weighted quantile sum regression,
• MeSH
• biologické markery * krev   MeSH
• dospělí MeSH
• látky znečišťující životní prostředí * krev   MeSH
• lidé středního věku MeSH
• lidé MeSH
• polychlorované bifenyly * krev   toxicita   MeSH
• senioři MeSH
• vystavení vlivu životního prostředí škodlivé účinky   analýza   MeSH
• výživa - přehledy * MeSH
• zánět krev   chemicky indukované   imunologie   MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• biologické markery * MeSH
• látky znečišťující životní prostředí * MeSH
• polychlorované bifenyly * MeSH

Since the 1960s, more than 350,000 new chemicals have been introduced into the lives of humans and domestic animals. Many of them have become part of modern life and some are affecting nature as pollutants. Yet, our comprehension of their potential health risks for both humans and animals remains partial. The "epithelial barrier theory" suggests that genetic predisposition and exposure to diverse factors damaging the epithelial barriers contribute to the emergence of allergic and autoimmune conditions. Impaired epithelial barriers, microbial dysbiosis, and tissue inflammation have been observed in a high number of mucosal inflammatory, autoimmune and neuropsychiatric diseases, many of which showed increased prevalence in the last decades. Pets, especially cats and dogs, share living spaces with humans and are exposed to household cleaners, personal care products, air pollutants, and microplastics. The utilisation of cosmetic products and food additives for pets is on the rise, unfortunately, accompanied by less rigorous safety regulations than those governing human products. In this review, we explore the implications of disruptions in epithelial barriers on the well-being of companion animals, drawing comparisons with humans, and endeavour to elucidate the spectrum of diseases that afflict them. In addition, future research areas with the interconnectedness of human, animal, and environmental well-being are highlighted in line with the "One Health" concept.

• Klíčová slova
• companion animals, epigenetics, epithelial barrier, exposome, microbiota, skin,
• MeSH
• domácí zvířata * imunologie   MeSH
• epitel imunologie   MeSH
• kočky MeSH
• lidé MeSH
• psi MeSH
• vystavení vlivu životního prostředí škodlivé účinky   MeSH
• zvířata MeSH
• Check Tag
• kočky MeSH
• lidé MeSH
• psi MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

Electronic waste (e-waste) poses significant environmental and health risks in Thailand due to both domestic production and international imports. A notable portion of this waste is processed in small-scale, community-based workshops, often located in poorer regions, where safety regulations are improperly enforced or entirely ignored. This study focuses on the Kalasin province in Northern Thailand, a region with numerous such workshops, where no comprehensive analysis of exposure to polybrominated diphenyl ethers (PBDEs) and dechlorane plus (DP) has been conducted. The study's objective was to quantify these toxic substances in environmental and biological samples to assess its contamination and human health risks. Environmental samples, including soil, dust, sediment, ash, eggs, crabs, snails, fish, and rice, were collected from e-waste processing sites and compared with control areas. Blood samples from e-waste workers and a control group were also analysed. Gas chromatography coupled with mass spectrometry operated in negative ion chemical ionization (GC-NCI-MS) was used to quantify PBDEs and DP isomers. Results showed significantly higher concentrations of these toxic compounds in e-waste sites compared to control areas. E-waste workers also had elevated levels of these substances in their blood, suggesting exposure through contaminated dust and food. These findings underscore the severe environmental contamination and health risks associated with improper e-waste management, highlighting the urgent need for regulatory measures and improved recycling practices to safeguard both environmental and public health.

• Klíčová slova
• Dechlorane plus, E-waste, Environmental pollution, Human health impact, POPs, Polybrominated diphenyl ethers,
• MeSH
• chlorované uhlovodíky * analýza   krev   MeSH
• elektronický odpad * analýza   MeSH
• halogenované difenylethery * analýza   toxicita   krev   MeSH
• hodnocení rizik MeSH
• látky znečišťující životní prostředí analýza   krev   MeSH
• lidé MeSH
• monitorování životního prostředí metody   MeSH
• polycyklické sloučeniny * analýza   MeSH
• prach analýza   MeSH
• pracovní expozice analýza   MeSH
• recyklace * MeSH
• vystavení vlivu životního prostředí škodlivé účinky   analýza   MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Geografické názvy
• Thajsko MeSH
• Názvy látek
• chlorované uhlovodíky * MeSH
• dechlorane plus MeSH Prohlížeč
• halogenované difenylethery * MeSH
• látky znečišťující životní prostředí MeSH
• polycyklické sloučeniny * MeSH
• prach MeSH

Industrial noise sources are among the environmental noise sources that are ranked second among the causes of ill health in Europe by the World Health Organization. The aim of this paper is to summarize and review of published information focusing on noise annoyance from industrial activities and mining. A search for articles was performed using the bibliographic databases platforms. The epidemiological evidence shows that environmental noise may be associated with cardiovascular and metabolic diseases, impaired cognitive development in children, mental health, post-irritability, and sleep disturbances. As a result of efforts to minimize the effects of industrial noise on human health, the New South Wales Environment Protection Authority published A Guide to the Noise Policy for Industry in 2017, which sets out recommended noise levels, methods, and procedures for noise management based on the latest scientific evidence. Social networks can be used to assess the population's noise annoyance and to verify the effectiveness of the measures. The industrial noise sources are typically defined by low-frequency noise. Low-frequency noise has very low attenuation and is only slightly affected by obstacles, therefore it can be a major cause of night noise annoyance. An association was confirmed between exposure to low-frequency noise and sleep disturbance, psychological problems, cognitive impairment, increased social conflicts, anxiety, emotional instability, nervousness, and reduced mental performance - concentration, and visual perception. In view of the long tradition of mining and industry, the assessment of noise from these activities from the perspective of its impacts on human health is an inherent part of legislative processes. Med Pr Work Health Saf. 2024;75(5):425-431.

• Klíčová slova
• environmental noise, health effects, industrial noise, low-frequency noise, noise annoyance, sleep disturbance,
• MeSH
• hluk na pracovišti škodlivé účinky   MeSH
• hluk * škodlivé účinky   MeSH
• lidé MeSH
• vystavení vlivu životního prostředí škodlivé účinky   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

BACKGROUND: Ambient air pollution, including particulate matter (such as PM10 and PM2·5) and nitrogen dioxide (NO2), has been linked to increases in mortality. Whether populations' vulnerability to these pollutants has changed over time is unclear, and studies on this topic do not include multicountry analysis. We evaluated whether changes in exposure to air pollutants were associated with changes in mortality effect estimates over time. METHODS: We extracted cause-specific mortality and air pollution data collected between 1995 and 2016 from the Multi-Country Multi-City (MCC) Collaborative Research Network database. We applied a two-stage approach to analyse the short-term effects of NO2, PM10, and PM2·5 on cause-specific mortality using city-specific time series regression analyses and multilevel random-effects meta-analysis. We assessed changes over time using a longitudinal meta-regression with time as a linear fixed term and explored potential sources of heterogeneity and two-pollutant models. FINDINGS: Over 21·6 million cardiovascular and 7·7 million respiratory deaths in 380 cities across 24 countries over the study period were included in the analysis. All three air pollutants showed decreasing concentrations over time. The pooled results suggested no significant temporal change in the effect estimates per unit exposure of PM10, PM2·5, or NO2 and mortality. However, the risk of cardiovascular mortality increased from 0·37% (95% CI -0·05 to 0·80) in 1998 to 0·85% (0·55 to 1·16) in 2012 with a 10 μg/m3 increase in PM2·5. Two-pollutant models generally showed similar results to single-pollutant models for PM fractions and indicated temporal differences for NO2. INTERPRETATION: Although air pollution levels decreased during the study period, the effect sizes per unit increase in air pollution concentration have not changed. This observation might be due to the composition, toxicity, and sources of air pollution, as well as other factors, such as socioeconomic determinants or changes in population distribution and susceptibility. FUNDING: None.

• MeSH
• kardiovaskulární nemoci * mortalita   MeSH
• látky znečišťující vzduch * škodlivé účinky   analýza   MeSH
• lidé MeSH
• nemoci dýchací soustavy * mortalita   chemicky indukované   MeSH
• oxid dusičitý * analýza   škodlivé účinky   MeSH
• pevné částice * analýza   škodlivé účinky   MeSH
• velkoměsta * MeSH
• vystavení vlivu životního prostředí škodlivé účinky   MeSH
• znečištění ovzduší * škodlivé účinky   analýza   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• Geografické názvy
• velkoměsta * MeSH
• Názvy látek
• látky znečišťující vzduch * MeSH
• oxid dusičitý * MeSH
• pevné částice * MeSH

The aim of this study was to investigate the relationship between source-specific ambient particulate air pollution concentrations and the incidence of dementia. The study encompassed 70,057 participants from the Västerbotten intervention program cohort in Northern Sweden with a median age of 40 years at baseline. High-resolution dispersion models were employed to estimate source-specific particulate matter (PM) concentrations, such as PM10 and PM2.5 from traffic, exhaust, and biomass (mainly wood) burning, at the residential addresses of each participant. Cox regression models, adjusted for potential confounding factors, were used for the assessment. Over 884,847 person-years of follow-up, 409 incident dementia cases, identified through national registers, were observed. The study population's average exposure to annual mean total PM10 and PM2.5 lag 1-5 years was 9.50 µg/m3 and 5.61 µg/m3, respectively. Increased risks were identified for PM10-Traffic (35% [95% CI 0-82%]) and PM2.5-Exhaust (33% [95% CI - 2 to 79%]) in the second exposure tertile for lag 1-5 years, although no such risks were observed in the third tertile. Interestingly, a negative association was observed between PM2.5-Wood burning and the risk of dementia. In summary, this register-based study did not conclusively establish a strong association between air pollution exposure and the incidence of dementia. While some evidence indicated elevated risks for PM10-Traffic and PM2.5-Exhaust, and conversely, a negative association for PM2.5-Wood burning, no clear exposure-response relationships were evident.

• MeSH
• demence * epidemiologie   etiologie   MeSH
• dospělí MeSH
• incidence MeSH
• kohortové studie MeSH
• látky znečišťující vzduch analýza   škodlivé účinky   MeSH
• lidé středního věku MeSH
• lidé MeSH
• pevné částice * analýza   škodlivé účinky   MeSH
• senioři MeSH
• vystavení vlivu životního prostředí * škodlivé účinky   MeSH
• znečištění ovzduší * škodlivé účinky   analýza   MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Geografické názvy
• Švédsko epidemiologie   MeSH
• Názvy látek
• látky znečišťující vzduch MeSH
• pevné částice * MeSH

BACKGROUND: Wildfire activity is an important source of tropospheric ozone (O3) pollution. However, no study to date has systematically examined the associations of wildfire-related O3 exposure with mortality globally. METHODS: We did a multicountry two-stage time series analysis. From the Multi-City Multi-Country (MCC) Collaborative Research Network, data on daily all-cause, cardiovascular, and respiratory deaths were obtained from 749 locations in 43 countries or areas, representing overlapping periods from Jan 1, 2000, to Dec 31, 2016. We estimated the daily concentration of wildfire-related O3 in study locations using a chemical transport model, and then calibrated and downscaled O3 estimates to a resolution of 0·25° × 0·25° (approximately 28 km2 at the equator). Using a random-effects meta-analysis, we examined the associations of short-term wildfire-related O3 exposure (lag period of 0-2 days) with daily mortality, first at the location level and then pooled at the country, regional, and global levels. Annual excess mortality fraction in each location attributable to wildfire-related O3 was calculated with pooled effect estimates and used to obtain excess mortality fractions at country, regional, and global levels. FINDINGS: Between 2000 and 2016, the highest maximum daily wildfire-related O3 concentrations (≥30 μg/m3) were observed in locations in South America, central America, and southeastern Asia, and the country of South Africa. Across all locations, an increase of 1 μg/m3 in the mean daily concentration of wildfire-related O3 during lag 0-2 days was associated with increases of 0·55% (95% CI 0·29 to 0·80) in daily all-cause mortality, 0·44% (-0·10 to 0·99) in daily cardiovascular mortality, and 0·82% (0·18 to 1·47) in daily respiratory mortality. The associations of daily mortality rates with wildfire-related O3 exposure showed substantial geographical heterogeneity at the country and regional levels. Across all locations, estimated annual excess mortality fractions of 0·58% (95% CI 0·31 to 0·85; 31 606 deaths [95% CI 17 038 to 46 027]) for all-cause mortality, 0·41% (-0·10 to 0·91; 5249 [-1244 to 11 620]) for cardiovascular mortality, and 0·86% (0·18 to 1·51; 4657 [999 to 8206]) for respiratory mortality were attributable to short-term exposure to wildfire-related O3. INTERPRETATION: In this study, we observed an increase in all-cause and respiratory mortality associated with short-term wildfire-related O3 exposure. Effective risk and smoke management strategies should be implemented to protect the public from the impacts of wildfires. FUNDING: Australian Research Council and the Australian National Health and Medical Research Council.

• MeSH
• celosvětové zdraví MeSH
• kardiovaskulární nemoci * mortalita   MeSH
• látky znečišťující vzduch * škodlivé účinky   analýza   MeSH
• lidé MeSH
• nemoci dýchací soustavy * mortalita   MeSH
• ničivé požáry * MeSH
• ozon * škodlivé účinky   analýza   MeSH
• vystavení vlivu životního prostředí škodlivé účinky   MeSH
• znečištění ovzduší škodlivé účinky   analýza   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• látky znečišťující vzduch * MeSH
• ozon * MeSH

Exposures to social and environmental stressors arise individual behavioural response and thus indirectly affect cardiometabolic health. The aim of this study was to investigate several social and environmental stressors and the paths of their influence on cardiometabolic health. The data of 2154 participants (aged 25-64 years) from the cross-sectional population-based study were analysed. The composite score of metabolic disorders (MS score) was calculated based on 5 biomarkers: waist circumference, blood pressure, fasting blood glucose, HDL-cholesterol, triglycerides. The effects of social stressors (education level, income), environmental stressors (NO2, noise) and behavioural factors (unhealthy diet, smoking, alcohol consumption, sedentary behaviours) on MS score were assessed using a structural model. We observed a direct effect of education on MS score, as well as an indirect effect mediated via an unhealthy diet, smoking, and sedentary behaviours. We also observed a significant indirect effect of income via sedentary behaviours. The only environmental stressor predicting MS was noise, which also mediated the effect of education. In summary, the effect of social stressors on the development of cardiometabolic risk had a higher magnitude than the effect of the assessed environmental factors. Social stressors lead to an individual's unhealthy behaviour and might predispose individuals to higher levels of environmental stressors exposures.

• MeSH
• biologické markery krev   MeSH
• dospělí MeSH
• HDL-cholesterol krev   MeSH
• kardiovaskulární nemoci etiologie   epidemiologie   MeSH
• kouření škodlivé účinky   MeSH
• krevní glukóza metabolismus   MeSH
• krevní tlak MeSH
• lidé středního věku MeSH
• lidé MeSH
• metabolické nemoci etiologie   epidemiologie   MeSH
• obvod pasu MeSH
• průřezové studie MeSH
• psychický stres MeSH
• rizikové faktory MeSH
• sedavý životní styl * MeSH
• triglyceridy krev   MeSH
• vystavení vlivu životního prostředí škodlivé účinky   MeSH
• Check Tag
• dospělí MeSH
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• biologické markery MeSH
• HDL-cholesterol MeSH
• krevní glukóza MeSH
• triglyceridy MeSH

This study investigates the potential relationship between exposure to polycyclic aromatic hydrocarbons (PAHs), specifically monohydroxylated metabolites (OH-PAHs), in urine, and the prevalence of respiratory diseases in 2-year-old children residing in two locations within the Czech Republic - České Budějovice (control location) and the historically contaminated mining district of Most. Despite current air quality and lifestyle similarities between the two cities, our research aims to uncover potential long-term health effects, building upon previous data indicating distinctive patterns in the Most population. A total of 248 urine samples were analysed for the presence of 11 OH-PAHs. Employing liquid-liquid extraction with ethyl acetate and clean-up through dispersive solid-phase extraction, instrumental analysis was conducted using ultra-high performance liquid chromatography coupled with tandem mass spectrometry. The incidence of respiratory diseases was assessed through questionnaires administered by paediatricians. The concentrations of OH-PAHs were elevated in urine samples from 2-year-olds in Most compared to those from České Budějovice. The incidence of respiratory diseases showed statistically significant higher levels of OH-PAHs in children from Most, together with a higher incidence of influenza. This association underlines the impact of environmental PAH exposure on children's respiratory health. It suggests that elevated urinary OH-PAH levels indicate an increased risk of developing respiratory diseases in the affected population. Further studies are needed to clarify the possible long-term health effects and to contribute to sound public health strategies.

• Klíčová slova
• 2-year-old toddlers, Influenza, Monohydroxylated PAH metabolites, Polycyclic aromatic hydrocarbons, Respiratory diseases, Urine,
• MeSH
• lidé MeSH
• nemoci dýchací soustavy epidemiologie   moč   MeSH
• pilotní projekty MeSH
• polycyklické aromatické uhlovodíky * moč   MeSH
• předškolní dítě MeSH
• vystavení vlivu životního prostředí škodlivé účinky   analýza   MeSH
• Check Tag
• lidé MeSH
• mužské pohlaví MeSH
• předškolní dítě MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• Geografické názvy
• Česká republika epidemiologie   MeSH
• Názvy látek
• polycyklické aromatické uhlovodíky * MeSH