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Chronic arsenic toxicity (arsenicosis) due to drinking of arsenic contaminated ground water is a major environmental health hazard throughout the world including India. A lot of new information is emerging from extensive research on health effects of chronic arsenic toxicity (CAT) in humans during the last two decades. Available literature has been...
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Context 1
... The nodular forms are encountered most frequently on the thenar and lateral borders of palms, on roots or lateral surfaces of fingers and soles, heels and toes of feet. Such small nodules may coalesce to form large verrucous lesions (Fig. 3). The nodular form may also occur in the dorsum of the hands and feet and other parts of the body (Fig. 4). In severe cases, cracks and fissures may be seen in the soles. Keratosis is further subdivided into mild, moderate and severe. Mild form appears as slight thickening or minute papules (less than 2 mm) in the palms and soles, often associated with a grit-like texture, which may be primarily detectable by palpation. Moderate forms are ...
Context 2
... a metalloid, occurs naturally, being the twentieth most abundant element in earth’s crust and is a component of more than 245 minerals. The inorganic forms consisting mostly of arsenite and arsenate compounds are toxic to human health. Humans are exposed to arsenic primarily from air, food and water. Drinking water may be contaminated with arsenic from arsenical pesticide, natural mineral deposits or improperly disposed arsenical chemicals. However, elevated arsenic level in drinking water is the major cause of arsenic toxicity in the world. Reports of arsenic contamination in water are available from more than 30 countries in the world 1 . However, the major regions affected are in the river basin of the Ganga, Brahmaputra and Meghna in India and Bangladesh with an estimated 25 million people in Bangladesh and 6 million people in West Bengal, India exposed to arsenic contaminated ground water 1 . In India, though cases of arsenic toxicity including liver fibrosis due to drinking of arsenic contaminated water were reported from Chandigarh in early 1978 2 , occurrence of large number of cases of arsenic induced skin lesions were reported from Kolkata, West Bengal in 1984 3 . Since then incidences of chronic arsenic toxicity have been reported in the most States adjoining the upper, middle and lower Ganga and Brahmaputra plain. Arsenic contamination has been found in the States of Bihar, Uttar Pradesh, Jharkhand, Assam, Chhattisgarh and Andhra Pradesh 4,5 . Human health effects of chronic arsenic toxicity (CAT) are designated by the term arsenicosis which was first coined by our group 6 and later used by WHO 7 to imply a chronic disease caused by prolonged exposure in humans to arsenic. Previously the condition was described as arseniasis, arsenism, arsenicism, etc . Most of the reports of chronic arsenic exposure in man focus attention on skin manifestations because of their diagnostic specificity. However, data derived from population based studies, clinical case series and reports relating to intake of inorganic arsenic in drinking water, medications or occupational and environmental exposure, show that chronic arsenic exposure adversely affects multi organ systems of human body. The symptoms of chronic arsenic toxicity (arsenicosis) are insidious in onset and are dependent on the magnitude of the dose and duration of its exposure. There is a wide variation of occurrence of symptoms in an arsenic exposed population. All members of an affected family do not show clinical symptoms, the reason for such variation of disease expression is an enigma. Pigmentation and keratosis are the specific skin lesions characteristic of chronic arsenic toxicity. The pigmentation of CAT commonly appears as a finely freckled, “raindrop” pattern that is particularly pronounced on the trunk and extremities distributed bilaterally symmetrically. The raindrop appearance results from the presence of numerous rounded hyperpigmented macules widely dispersed in the body (Fig. 1). Pigmentation might also involve mucous membranes such as undersurface of tongue or buccal mucosa. Other patterns include diffuse hyperpigmentation, localized patchy pigmentation, and leucomelanosis, in which the hypopigmented macules take on a spotty white appearance (Fig. 2). Leucomelanosis appears to occur in an arsenicosis patient following stoppage of drinking arsenic contaminated water for some duration 8-10 . Arsenical keratosis appears as diffuse thickening involving palms and soles, alone or in combination with nodules usually symmetrically distributed. The nodular forms are encountered most frequently on the thenar and lateral borders of palms, on roots or lateral surfaces of fingers and soles, heels and toes of feet. Such small nodules may coalesce to form large verrucous lesions (Fig. 3). The nodular form may also occur in the dorsum of the hands and feet and other parts of the body (Fig. 4). In severe cases, cracks and fissures may be seen in the soles. Keratosis is further subdivided into mild, moderate and severe. Mild form appears as slight thickening or minute papules (less than 2 mm) in the palms and soles, often associated with a grit-like texture, which may be primarily detectable by palpation. Moderate forms are multiple raised keratotic lesions (2-5 mm) while severe forms are large discreate or confluent elevations (>5 mm) on palms and soles, with nodular, wart-like or horny appearance 7,10 . Histological examination of the lesions typically reveals hyperkeratosis with or without parakeratosis, acanthosis, and enlargement of the rete ridges. In some cases, there might be evidence of cellular atypia, mitotic figure, in large vacuolated epidermal cells 11 . To ascertain the prevalence of keratosis and pigmentation in relation to arsenic exposure, first population based survey was carried out on 7683 participants (4093 female and 3590 male) in West Bengal with individual arsenic exposure data 9 . Arsenic content of water source of the participants ranged from BDL (below detection limit) to 3.4 mg/l, however over 80 per cent of participants consumed water with arsenic level <0.5 mg/l. The age-adjusted prevalence of keratosis and pigmentation was strongly related to water arsenic levels, rising from zero and 0.3 in the lowest exposure level (<0.05 mg/l), to 8.3 and 11.5 per 100 respectively for females drinking water containing >0.8 mg/l, and increasing from 0.2 and 0.4 per 100 in the lowest exposure category to 10.7 and 22.7 per 100 respectively for males in the highest exposure level (>0.8 mg/l). Calculation by dose per body weight showed that men had roughly two to three times the prevalence of both keratosis and pigmentation compared to women apparently ingesting the same dose of arsenic from drinking water. Subjects who were below 80 per cent of the standard body weight for their age and sex had a 1.6 fold increase in the prevalence of keratosis suggesting that malnutrition may play some role in increasing susceptibility. However, the survey examined only the participants’ primary current drinking water source. Results of a nested case control study using detailed lifetime (at least 20 yr) exposure assessment having low dose of arsenic exposure (<0.5 mg/l) among the above mentioned study population were also available 12 . The exposure assessment incorporated arsenic concentration data from current and past water sources used in households and work sites. The lowest peak arsenic ingested by a confirmed case was 0.115 mg/l. Strong dose response gradients with both peak and average arsenic water concentrations were also observed 12 . In another cross-sectional study, conduced in Bangladesh, 430 out of 1,481 subjects aged > 30 yr and drinking arsenic contaminated water were found to have arsenical skin lesions. Arsenic water concentrations ranged from 0.01 to 2.04 mg/l and the crude overall prevalence rate for skin lesions was 29 per cent. This study also showed a higher prevalence rate of arsenical skin lesions in males than females with clear dose-response relationship 13 . Chronic arsenic toxicity produces various systemic manifestations over and above skin lesions. This was evident from the report of the clinical features in 156 cases chronically drinking arsenic-contaminated water in West Bengal, India (Table) 14 . Initial report of non malignant lung disease was available from a study of 180 residents of Antofagasta, Chile, exposed to drinking water containing arsenic (0.8 mg/l). About 38 per cent of 144 subjects with abnormal skin pigmentation complained of chronic cough, compared with 3.1 per cent of 36 subjects with normal skin 15 . Symptoms of chronic lung disease were present in 89 (57%) out of 156 cases of chronic arsenic toxicity caused by drinking arsenic contaminated water in West Bengal 14 . Lung function tests carried out on 17 patients showed features of restrictive lung disease in 9 (53%) and combined obstructive and restrictive lung disease in 7 (41%) cases 14 . To ascertain the relation of chronic arsenic exposure on occurrence of lung disease, an analysis of data of cross-sectional epidemiological survey of non smokers (6,864 participants) was carried out in West Bengal. Study subjects included those who had arsenic associated skin lesion and who were also highly exposed at the time of the survey (arsenic water concentration >0.5 mg/l). Individuals with normal skin and low arsenic water concentration (<0.05 mg/l) were used as the referent group. In participants with skin lesions, the age adjusted prevalence odds ratio (POR) estimates for cough, crepitations and shortness of breath for females were 7.8, 9.6 and 23.2 and for males 5, 6.9 and 3.7 respectively 16 . In an epidemiological study carried out on 218 non smokers (94 exposed to arsenic, 0.136 to 1 mg/l and 124 unexposed cases) in Bangladesh, the crude prevalence ratios for chronic bronchitis were ...
Citations
... One potential tactic to avert the negative consequences of chronic liver disease is to prevent liver fibrosis [9]. According to morphological and clinical investigations, liver fibrosis is a significant morphological lesion in patients with chronic arsenic poisoning [10]. Patients with liver fibrosis have been found in populations with arsenic poisoning in Bangladesh [4,11] and China [12]. ...
Arsenic is an environmental pollutant that has garnered considerable attention from the World Health Organization. Liver fibrosis is an advanced pathological stage of liver injury that can be caused by chronic arsenic exposure and has the potential to be reversed to prevent cirrhosis and hepatic malignancies. However, effective treatment options are currently limited. Given the profibrogenic effect of hepatocyte senescence, we established a rat model of sub-chronic sodium arsenite exposure and investigated the ability of resveratrol (RSV), a potential anti-senescence agent, to ameliorate arsenic-induced liver fibrosis and elucidate the underlying mechanism from the perspective of hepatocyte senescence. The results demonstrated that RSV was capable of mitigating fibrosis phenotypes in rat livers, including the activation of hepatic stellate cell (HSC), the generation of extracellular matrix, and the deposition of collagen fibers in the liver vascular zone, which are all induced by arsenic exposure. Furthermore, as an activator of the longevity factor SIRT1, RSV antagonized the arsenic-induced inhibition of SIRT1 expression, thereby restoring the suppression of the senescence protein p16 by SIRT1. This prevented arsenic-induced hepatocyte senescence, manifesting as a decrease in telomere shortening and a reduction in the release of senescence-associated secretory phenotype (SASP)-related proteins. In conclusion, this study demonstrated that RSV counteracts arsenic-induced hepatocyte senescence and the release of SASP-related proteins by restoring the inhibitory effect of SIRT1 on p16, thereby suppressing the activation of fibrotic phenotypes and mitigating liver fibrosis. These findings provide new insights for understanding the mechanism of arsenic-induced liver fibrosis, and more importantly, they reveal novel potential interventional approaches.
... In addition, both As and Cr pose a significant risk to children with an average value of 4.43E-03 and 1.16E-03, respectively, while only as poses a significant risk to adults from dermal ingestion in the south-central zone. Lung and skin cancers frequently occur with prolonged exposure to as (Mazumder 2008;Varol et al. 2020). Therefore, there is a potential due to combined exposure from ingestion and skin contact with water contaminants. ...
Despite sporadic and irregular studies on heavy metal(loid)s health risks in water, fish, and soil in the coastal areas of the Bay of Bengal, no chemometric approaches have been applied to assess the human health risks comprehensively. This review aims to employ chemometric analysis to evaluate the long-term spatiotemporal health risks of metal(loid)s e.g., Fe, Mn, Zn, Cd, As, Cr, Pb, Cu, and Ni in coastal water, fish, and soils from 2003 to 2023. Across coastal parts, studies on metal(loid)s were distributed with 40% in the southeast, 28% in the south-central, and 32% in the southwest regions. The southeastern area exhibited the highest contamination levels, primarily due to elevated Zn content (156.8 to 147.2 mg/L for Mn in water, 15.3 to 13.2 mg/kg for Cu in fish, and 50.6 to 46.4 mg/kg for Ni in soil), except for a few sites in the south-central region. Health risks associated with the ingestion of Fe, As, and Cd (water), Ni, Cr, and Pb (fish), and Cd, Cr, and Pb (soil) were identified, with non-carcinogenic risks existing exclusively through this route. Moreover, As, Cr, and Ni pose cancer risks for adults and children via ingestion in the southeastern region. Overall non-carcinogenic risks emphasized a significantly higher risk for children compared to adults, with six, two-, and six-times higher health risks through ingestion of water, fish, and soils along the southeastern coast. The study offers innovative sustainable management strategies and remediation policies aimed at reducing metal(loid)s contamination in various environmental media along coastal Bangladesh.
... It is one of the top twenty most abundant elements in the earth's crust and a component of over 245 minerals. The inorganic form consists mainly of arsenic and arsenate compounds, which are toxic to human health [1] . Human exposure to arsenic primarily occurs through air, food and drinking water -most likely from arsenic-containing pesticides, natural mineral deposits or improperly disposed arsenical chemicals [1] . ...
... The inorganic form consists mainly of arsenic and arsenate compounds, which are toxic to human health [1] . Human exposure to arsenic primarily occurs through air, food and drinking water -most likely from arsenic-containing pesticides, natural mineral deposits or improperly disposed arsenical chemicals [1] . ...
... Arsenic exposure also impairs intellectual reasoning in children, increases morbidity, decreases the quality of life and, ultimately, causes mortality in adults [3,2,1] . Trivalent arsenic toxicity can occur directly by attacking -SH groups or indirectly by generating reactive oxygen species (ROS) [4] . ...
Exposure to arsenic from drinking water poses a significant threat to public health worldwide. Clerodendrum volubile and Vernonia amygdalina are potent natural sources of antioxidants to mitigate the toxic effect of arsenic. This study evaluated the effects of flavonoid fractions from C. volubile and V. amygdalina (FICV and FIVA) on the thiol cycling pathways and ion regulation of male albino rats exposed to sub-acute arsenic. Thirty male rats were randomly divided into six treatment groups. Control animals (distilled water), arsenic (40 ppm arsenic), arsenic + FICV (100 mg/ kg), arsenic + FIVA (100 mg/kg), arsenic + FICV and FIVA (50 mg/kg each) and arsenic + Vitamin C (100 mg/kg). The treatment commenced four weeks after exposure to arsenic in drinking water and continued for a further four weeks. The liver and kidneys of the rats were excised following an overnight fast. Arsenic had caused significant (p<0.05) reductions in the total protein levels and metallothionein levels, reduced glutathione levels in the liver and kidneys, and decreased glutathione-S-transferase enzymatic activity. Additionally, essential elements (magnesium, zinc, copper and calcium) were significantly reduced (p<0.05) in the arsenic-exposed rats. Study results showed that the reductions were reversed after treatment with FICV and FIVA. This study concludes that flavonoid fractions from C. volubile and V. amygdalina possess potent therapeutic actions against arsenic-induced oxidative stress and toxicity in male albino rats.
... Chronic arsenic exposure through drinking water to humans leads to carcinogenesis of almost all organs, skin diseases (viz. hyper-pigmentation, hyperkeratosis) leading to cancers of skin and epithelial tissues; hepatic, renal, cardiovascular, respiratory, central nervous system, gastrointestinal, reproductive complications, and children's intellectual impairment; thereby increasing morbidity and mortality (Kapaj et al., 2006;Mazumder, 2008;Khatun et al., 2020). ...
This study was undertaken to observe the effects of Thankuni and grapes on hematological and biochemical parameters against arsenicosis in Long Evans rats. Sixty male rats were selected to perform the study. The experimental rats were randomly divided into five different groups, with n = 12 in each group. Animals in group T0 were given normal feed and water and kept as control. Rats of group T1 were given arsenic trioxide @ 100 mg/L of drinking water orally. Rats of group T2 were given arsenic trioxide @ 100 mg/L drinking water and Thankuni @ 1gm/kg feed. Group T3 was given arsenic trioxide @ 100 mg/L drinking water with grapes @ 10 mg /kg body weight thrown DW. Group T4 was given arsenic trioxide, Thankuni, and grapes with the same dose for up to 45 days, respectively. Four randomly selected rats from each group (T0, T1, T2, T3, and T4) were sacrificed at 15-day intervals to determine body weight, hematological and biochemical parameters. At the end of the experiment, the result showed that the minimum weight gain group was T1 whereas the maximum weight gain was found in the T3 and T4 groups. The weight gain of the T2 group is better than T1. Reduction of TEC and Hb values were significant (P < 0.01) in the T1 group. Whereas in the rest of the groups, the reduction of TEC and Hb was less than in arsenic-treated groups. In conclusion, Thankuni and grapes have a significant effect on body weight and hematological and biochemical parameters.
... The contamination of drinking water can occur due to the application of arsenical pesticides, the presence of natural mineral deposits, or the disposal of arsenical substances. The intentional ingestion of arsenic in situations of suicide attempts or unintentional ingestion by children can also lead to acute poisoning [104,105]. Arsenic toxicity is a major public health concern. Humans are exposed to arsenic mostly through the ingestion of contaminated water and food as well as through occupational activities. ...
Polysaccharides are functional foods or drugs that can be used to alleviate heavy metal poisoning by cadmium, lead, mercury, and arsenic. Industries generate substantial quantities of toxic heavy metal wastes, such as wastewater discharges, paints, electronic waste, batteries, pigments, and plastics, into the environment that pose a risk to human health. Therefore, it is imperative to eliminate accumulated heavy metal ions from the body and the environment. Heavy metal toxicity can lead to decreased energy levels and impair the functioning of vital organs, such as the brain, lungs, kidneys, liver, and blood. Prolonged exposure can result in progressive physical, muscular, and neurological degeneration that resembles conditions such as multiple sclerosis, Parkinson’s disease, Alzheimer’s disease, and muscular dystrophy. Polysaccharides operate through mechanisms such as chelation, antioxidant defense, immunomodulation, and tissue repair. Polysaccharides involved in heavy metal removal include methionine and cysteine, together with N-acetylcysteine, an acetylated form of cysteine, S-adenosylmethionine, a metabolite of methionine, α-lipoic acid, and the tripeptide glutathione (GSH). These compounds effectively bind with harmful heavy metals to create a stable complex and defend biological targets from metal ions, thus decreasing their harmful effects and causing them to be excreted from the body. This review also highlights the importance of polysaccharides’ ability to mitigate oxidative stress, enhance immune responses, and support tissue repair processes. Polysaccharides are ubiquitous in nature and take part in diverse processes, making them potential natural therapies for heavy metal-related diseases. This review discusses the effectiveness of natural polysaccharides and the mechanisms that allow them to bind with heavy metals to alleviate their effects from the body and the environment. Polysaccharides have inherent features that enable them to function as pharmacological agents and regulate the immune response.
... Dear Editor, Arsenic keratosis is characterized by guttate skin hyperpigmentation and hypopigmentation, and multiple punctate corn-like yellowish hyperkeratotic papules and plaques predominantly involving the palms and soles resulting from ingestion of arsenic above the safe limit (50 µg/L) for a period of minimum 6 months and lesions may progress to Squamous cell carcinoma and Basal cell carcinoma and other internal organ malignancies like lung, bladder, kidney, and GIT. [1,2] Inorganic arsenic has been classified as a class 1 human carcinogen with contaminated groundwater, medications, occupation, and tobacco consumption to be the sources of exposure. [3] Diagnosis is through clinical examination, estimation of blood, urine, hair and nail arsenic levels, and histopathology. ...
... Pb induces toxicity through ionic mechanisms and oxidative stress, while Hg is highly toxic and bioaccumulates (Chen et al., 2012). Cd is identified as the seventh most toxic element (Järup, 2003;Irfan et al., 2013), disrupting cell functions like respiration, enzymes, and mitosis by affecting sulfhydryl groups (Guha Mazumder, 2008;Choi et al., 2010;Wadhwa et al., 2012). ...
Consumption of fish and shellfish exposed to high levels of pollutants from environmental sources and anthropogenic activities can lead to the accumulation of toxic elements in humans. Mercury (Hg), cadmium (Cd), lead (Pb), and arsenic (As) can cause serious health problems in consumers of all ages. This study examined toxic element levels and associated health risks in gilthead seabream, European seabass, and Mediterranean mussels from aquaculture farms which represent commercially important species exported from Türkiye. Fifty-one samples were analysed for Hg, Cd, Pb, and As. In general, the annual average concentrations of toxic elements in seabream, seabass, and mussel samples were generally below the established limits. On a seasonal basis, it was determined that the limit value for Cd recommended by the EU (0.05 mg/kg) was exceeded for sea bream and sea bass species of only one farm, with values of 0.080–0.088 mg/kg, respectively, in the summer season. The Total Target Hazard Quotients (TTHQ) and Target cancer Risk (TR) indexes were calculated for the European Union (EU) and Turkish populations to assess consumer health and safety. Consequently, fish and mussel samples obtained from aquaculture farms were highly reliable and found to be safe for consumption. The exceeding of Cd levels in fish beyond the established limit in a single season on one farm demonstrates the necessity for regular monitoring of parameters.
... This leads to the development of arsenic induced skin lesions which are the hall marks of chronic arsenic toxicity. Other detrimental health effects include cancers of the internal organs, peripheral neuropathy, respiratory distress, conjunctivitis of the eyes, cardiovascular disease, diabetes mellitus and liver diseases (Guha Mazumder 2008). Altered miRNA expression profiles have been associated with various diseases including cancers (Calin & Croeci 2006). ...
... The epidemiological data show that chronic arsenic exposure can cause abnormal liver function, fibrosis, cirrhosis, and liver cancer [5][6][7][8]. Among them, clinical and morphological studies have found liver fibrosis to be an important morphological lesion associated with chronic arsenic toxicity [9][10][11]. Liver fibrosis is a reversible pathological stage in the progression of liver injury and chronic liver disease to cirrhosis and liver cancer, and it is critical to prevent the adverse outcomes of chronic liver disease during this period [12]. ...
Arsenic pollution is a global environmental concern. Arsenic-induced chronic liver injury and its irreversible outcomes, including liver cirrhosis and liver cancer, threaten the health of residents in arsenic-contaminated areas. Liver fibrosis is a reversible pathological stage in the progression of arsenic-induced chronic liver injury to cirrhosis and liver cancer. The aim of this study is to identify the epigenetic mechanism of arsenic-induced liver fibrosis based on the dedifferentiation of liver sinusoidal endothelial cells (LSECs). Rats were treated with 0.0, 2.5, 5.0, or 10.0 mg/kg sodium arsenite for 36 weeks. Marked fibrotic phenotypes were observed in the rat livers, manifested by hepatic stellate cell activation and an increased extracellular matrix, as well as the deposition of collagen fibers. The reduced fenestrations on the cells’ surface and the increased expression of the dedifferentiation marker CD31 corroborated the LSECs’ dedifferentiation in the liver tissue, which was also found to be significantly associated with fibrotic phenotypes. We further revealed that arsenic exposure could inhibit the enrichment of histone H3 lysine 18 acetylation (H3K18ac) in the promoters of Fcgr2b and Lyve1, two key genes responsible for maintaining the differentiation phenotype of LSECs. This inhibition subsequently suppressed the genes’ expression, promoting LSEC dedifferentiation and subsequent liver fibrosis. In conclusion, arsenic can trigger liver fibrosis by inhibiting H3K18ac-dependent maintenance of LSEC differentiation. These findings uncover a novel mechanism of arsenic-induced liver fibrosis based on a new insight into epigenetically dependent LSEC dedifferentiation.
... Underground sources of potable water are widely recognized as a primary contributor responsible for the chronic health problems related to arsenic poisoning of the population worldwide. Arsenic in drinking water sources is primarily found as As(V) and more frequently as As(III), with the latter being even more toxic [4,[7][8][9][10][11]. ...
The remediation of arsenic contamination in potable water is an important and urgent concern, necessitating immediate attention. With this objective in mind, the present study investigated arsenic removal from water using batch adsorption and fixed-bed column techniques. The material employed in this study was a waste product derived from the treatment of groundwater water for potable purposes, having a substantial iron composition. The material’s properties were characterized using scanning electron microscopy (SEM), energy-dispersive X-ray spectroscopy (EDX), and Fourier-transformed infrared spectroscopy (FT-IR). The point of zero charge (pHPZC) was measured, and the pore size and specific surface area were determined using the BET method. Under static conditions, kinetic, thermodynamic, and equilibrium studies were carried out to explore the influencing factors on the adsorption process, namely the pH, contact time, temperature, and initial arsenic concentration in the solution. It was found that the adsorption process is spontaneous, endothermic, and of a physical nature. In the batch adsorption studies, the maximum removal percentage was 80.4% after 90 min, and in a dynamic regime in the fixed-bed column, the efficiency was 99.99% at a sludge:sand = 1:1 ratio for 380 min for a volume of water with arsenic of ~3000 mL. The kinetics of the adsorption process conformed to a pseudo-second-order model. In terms of the equilibrium studies, the Sips model yielded the most accurate representation of the data, revealing a maximum equilibrium capacity of 70.1 mg As(V)/g sludge. For the dynamic regime, the experimental data were fitted using the Bohart–Adams, Thomas, and Clark models, in order to establish the mechanism of the process. Additionally, desorption studies were conducted, serving as an essential step in validating the practical applicability of the adsorption process, specifically in relation to the reutilization of the adsorbent material.
