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Abstract

Human exposure to heavy metals is a worldwide major health problem. Heavy metals which cause neurological toxicity, such as Pb, Hg, Cd, Cu, Zn, As, Fe and Cd consideredas most neurotoxic agent which affect humans. They having particular concern due to the long-lasting and possibly irreversible nature of their effects. The heavy metal exposure in childhood can result in cognitive and behavioral deficits in children.Neurotoxicological disorders such as autism, attention deficit disorder, mental retardation, and cerebral palsy are common but dangerous as it can cause lifelong disability. Metals are universal and take dangerous part in neurobiology. Heavy metals generate toxic effects on different organs of body and by this differently affect Humans. Heavy metals contaminate in water, air, soil etc. and affect human beings by different ways.
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Heavy Metal Causing Neurotoxicity in Human
Health
Mahipal Singh Sankhla1, Kirti Sharma2, Dr. Rajeev Kumar2
Student of M.Sc. Forensic Science, Division of Forensic Science, Galgotias University, Greater Noida, India1
Student of M.Sc. Forensic Science, Department of Biotechnology, Baba Saheb Bhimrao Ambedkar University,
Lucknow, India 2
Assistant Professor, Division of Forensic Science, Galgotias University, Greater Noida, India 3
ABSTRACT: Human exposure to heavy metals is a worldwide major health problem. Heavy metals which cause
neurological toxicity, such as Pb, Hg, Cd, Cu, Zn, As, Fe and Cd consideredas most neurotoxic agent which affect
humans. They having particular concern due to the long-lasting and possibly irreversible nature of their effects. The
heavy metal exposure in childhood can result in cognitive and behavioral deficits in children.Neurotoxicological
disorders such as autism, attention deficit disorder, mental retardation, and cerebral palsy are common but dangerous as
it can cause lifelong disability. Metals are universal and take dangerous part in neurobiology. Heavy metals generate
toxic effects on different organs of body and by this differently affect Humans. Heavy metals contaminate in water, air,
soil etc. and affect human beings by different ways.
KEYWORDS: -Neurotoxicity, Heavy Metal, Effect, etc.
I. INTRODUCTION
Heavy metal poisoning has become an increasingly major health problem, especially since the industrial revolution,
effect may be either acute or chronic [1, 2]. Additionally, mental disability prevalence rates were twice as high in
developing countries as found in developed countries. Environmental factors, such as maternal and child health care,
immunizations, and environmental pollution, can influence the prevalence of mental disability [3].Thus, poorer health
quality and higher contamination levels of pollutants in developing countries may contribute to the higher prevalence
rates. A prime agent implicated in cognitive and neurological deficits is environmental exposure to heavy metals.
Heavy metal exposure can occur through contaminated air, food, water, or in hazardous occupations. While the levels
of heavy metal contamination of the environment have decreased in recent decades in the developed world, the
developing world experiences high levels of metal pollution. In particular, Asian and African countries have high levels
of metal contamination, especially in urban environments [4, 5]. The excess quantities of heavy metals are detrimental
as these destabilize the ecosystems because of their bioaccumulation in organisms, and elicit toxic effects on biota and
even death in most living organisms [6]. Nearly all organ systems are involved in heavy metal toxicity; however, the
most commonly involved systems include the (central nervous system) CNS, (peripheral nervous system) PNS,
hematopoietic, renal, and cardiovascular. The other problems include carcinogeni city, nephrotoxicity, nervous system
toxicity, respiratory system toxicity, endocrine and reproductive effects [7]. With prenatal or neonatal developmental
insults, dietary deficits and stress damage the brain structures and down regulate essential neurotransmitters, because
toxic metals are retained in bone urine, feces and astroglial cells in the brain [8]. Small amounts of toxic metals appear
in hair, nails, sweat, saliva and breast milk [9, 10]. Uptake during fetal development and early childhood has long
lasting effects on development and behavior. Although ligand formation is the basis for much of the transport of heavy
metals throughout the body, some metals may compete with ionized species such as calcium and zinc to move through
membrane channels in the free ionic form.For example, lead follows calcium pathways in the body [11, 12, 13].
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Neurotoxicity of Iron (Fe)
Iron(Fe) and neurodevelopment has focused primarily on the effects of Fe deficiency anemia. Nevertheless, there is
evidence that excess Fe stores in pregnancy and newborns may be toxic. Several studies have noted a ‘‘U’’-shaped
association between maternal hemoglobin or serum ferritin (SF) and low birth weight. This association has been
attributed by some investigators to a failure of normal plasma volume expansion in pregnancyor to inflammation from
undiagnosed perinatal infection, as serum ferritin is a well-known acute-phase reactant [14, 15]. Showed that high
trimester-2 maternal Fe stores not only predicted low birth weight and prematurity but also predicted decreases in IQ in
children who were followed until age 5 y. More recently [16].Demonstrated a U-shaped association between infant
umbilical cord SF and lower IQ scores at age 5 y in an Alabama birth cohort. Subjects in the highest quartile of SF at
birth were 3.3-fold more likely than the middle 2 quartiles (95% confidence interval: 1.2–9.1) to score below the 15th
percentile in full-scale IQ. Similar findings were reported for subjects in the lowest quartile for SF, suggesting that both
high and low Fe stores are associated with poor developmental outcomes. Animal studies also support these findings.
Fe supplementation of rats produced a decrease in motor activity and exploratory and stereotyped behaviors similar to
that of late iron deficiency (ID) anemia [17]. Another report by Fredriksson et al. showed that mice administered large
oral doses of Fe at postnatal d 10–12 had long-term effects on spontaneous motor behavior, with the animals showing a
lack of habituation of spontaneous activity and poorer performance in the radial maze test at 3 mo of age [18]. Such
findings, if validated, will undoubtedly complicate public health efforts at eradicating Fe deficiency but should not be
dismissed as confounding from the effects of ferritin as an acute phase reactant. Excess Fe is known to be neurotoxic in
adults, and the possibility that it may also produce health effects in pregnant women and newborns must also be
investigated [19].
Neurotoxicity of Lead (Pb)
The lead exposure is a public health concern, especially in early childhood as children are more at risk because of
increased hand to mouth activity and absorb about half of an oral dose of water-soluble lead [20]. Childhood lead
exposure is estimated to contribute to 600,000 new cases of children with intellectual disabilities every year with
99 % of them living in developing countries [21]. The lead exposure in utero, infancy or early childhood can slow
mental development and cause lower intelligence later in childhood that can persist beyond childhood. The effects of
lead are more toxic on developing nervous system of children than on a mature brain. Lead-associated deficits have
been documented in most fields including verbal intelligence quotient (IQ), performance IQ, academic skills such as
reading and mathematics, visual/spatial skills, problem-solving skills, executive functions, fine and gross motor
skills, memory and language skills. Meta-analyses have indicated that children’s IQ scores decline 2–3 points per 10
ug/dl increase in blood lead level and identified no threshold for the effects of lead on IQ [22, 23]. In fact academic
performance of children exposed to lead has been observed to be subservient in comparison to controls. Children (6–
10 year old) with blood lead levels of 5–10 ug/dl scored significantly lower than children with levels of 1–2 ug/dl on
academic skills such as word reading, reading comprehension, listening comprehension, math reasoning and math
calculations [22]. Another large American study documented inverse association between blood lead levels as low as
2 ug/dl, measured up to 5 years of age, and end-of-grade reading and mathematics achievement scores [24]. In
National Health and Nutrition Examination Survey (1999–2002), the risk of parent-reported diagnosis of attention
deficit hyperactivity disorder increased, in a dose-dependent manner with blood lead level [22]. Similar findings
have been reported by a recent Indian study which emphasizes the detrimental effect of lead on executive and
attention domain in neurobehavioral function [25]. The mechanisms underlying lead-induced neurotoxicity are
complex. Oxidative stress, membrane bio-physics alterations, deregulation of cell signaling, and the impairment of
neurotransmission are key aspects involved in lead neurotoxicity. It can cause toxicity by oxidative stress directly or
indirectly by lipid peroxidation resulting in the generation of reactive oxygen species (ROS), including
hydroperoxides, singlet oxygen, hydrogen peroxide and direct depletion of antioxidant reserves. Lead renders
enzymes nonfunctional by binding to their sulfhydryl groups further contributing to an impairment in oxidative
balance [26]. The ability of lead to pass through the blood–brain barrier is mainly due to its ability to substitute for
calcium ions. Within the brain, lead-induced damage in the prefrontal cerebral cortex, hippocampus, and cerebellum
can lead to a variety of neurological disorders, such as brain damage, mental retardation, behavioral problems, nerve
damage, and possibly Alzheimer’s disease, Parkinson’s disease and schizophrenia [27]. Lead substitutes for calcium
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and to a lesser extent zinc, inappropriately triggers processes dependent on calmodulin. Lead also restricts
neurotransmitter release, disrupting the function of GABAergic, dopaminergic and cholinergic systems as well as
inhibiting NMDA-ion channels during the neonatal period. Indeed experimental studies have shown that lead
activates protein kinase C in capillary cells and inhibits Na+/K+-ATPase thus interfering with energy metabolism.
Within the cell, lead appears to interfere with calcium release from the mitochondria resulting in formation of
permeability transition pore and primes for programmed cell death processes leading to mitochondrial self-
destruction [28]. Hence direct neurotoxic actions of lead include apoptosis, excitotoxicity affecting neurotransmitter
storage, release and modifying neurotransmitter receptors, mitochondria, second messengers, cerebrovascular
endothelial cells, astroglia and oligodendroglia. Mechanisms underlying cognitive deficits resultant of lead exposure
have been reported using cellular models of learning and memory. There is convincing evidence that exposures to
lead have adverse effects on the central nervous system (CNS), environmental factors augment lead susceptibility
and exposures in early life can cause neurodegeneration in later life. Magnetic resonance spectroscopy (MRS) has
revealed reductions in the N-acetylaspartate-to-creatine and phosphocreatine ratios in the frontal gray matter of lead-
exposed children, consistent with increased neuronal loss. Similarly in adults an association between greater
cumulative lead exposure and higher myoinositol-to-creatine ratios in the hippo-campus, reflecting glial dysfunction
has been seen [22].
Neurotoxicity of Copper (Cu) and Zinc(Zn)
Like Fe, most of the literature on the neurotoxicity of Cu and Zn centers around nutritional deficiency and its effect on
brain [29]. Also, as for Fe, there is evidence of neurotoxicity when these metals are found in excess in the brain. Cu is a
transition metal, and consequently, its metabolism and toxicity are similar to those of Fe and Mn. As for Fe, genetic
diseases of excess Cu retention are well described and have significant neurologic sequelae. Wilson’s disease is the
most common of these diseases, and the presenting complaint for this genetic disorder frequently includes
neurobehavioral changes resembling schizophrenia [30]. These neurologic findings may even precede other findings
such as liver disease. Descriptions of environmental or excess dietary Cu producing subclinical neurobehavioral effects
are very rare, but these have not been systematically studied. Excess brain Cu is a common finding in
neurodegenerative diseases such as Alzheimer’s disease. Zn deficiency has long been known to impact
neurodevelopment adversely, but the effects of excess Zn on neurodevelopment are essentially unknown. Excess Zn,
like excess Fe and Cu, is a common finding in neurodegenerative disease [31]. Zn finger proteins are key
transcriptional elements that regulate the cellular response to metal toxicity among other processes. Excess Zn is
involved in the neuronal injury observed in cerebral ischemia, epilepsy, and brain trauma. Toxic Zn accumulation may
result from either trans synaptic Zn movement or mobilization from intracellular sites, such as Zn flux through receptor
associated calcium channels, voltage-sensitive calcium channels, or Zn-sensitive membrane transporters [32]. The
mechanisms by which Zn exerts its neurotoxicity include mitochondrial production of reactive oxygen species and the
disruption of metabolic enzymes, ultimately leading to activation of apoptotic processes. As with Cu, Fe, and Mn, an
exciting new area of research is the role of Zn metabolism in Alzheimer’s disease as a trigger for amyloid-b
aggregation and neuronal plaque formation. As we previously noted, excess Fe, particularly during pregnancy, has been
associated with neurodevelopmental outcomes later in life, and similar studies of Cu and Zn in pregnancy are sorely
needed [19].
Neurotoxicity of Cd
The neurotoxicity of Cd in children was investigated in severalstudies in the 1970s and 1980s but has received little
attention since. In most of these studies, the biomarker of exposure was the concentration of Cd in hair. In case-control
studies in which the hair concentration of Cd of a clinically defined group was commonly encountered as mixtures in
the environment. Initial studies merely reported correlations among markers of internal metal dose, including a positive
correlation between blood Pb and Mn and a positive correlation between urine As and blood Pb among children [33-
35].With respect to neurologic outcomes, we are unaware of any clinical data investigating joint exposures to Mn and
Pb. However, animal studies provide compelling evidence that exposure to both Mn and Pb lead to synergistic
neurological effects. Among rats orally exposed to both Mn and Pb, motor activity and neurotransmitter levels were
significantly increased, compared with rats exposed to only 1 metal [36].Exposure to Pb and Mn decreased learning of
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conditioned avoidance responses more than either Pb or Mn alone, and gestational exposure to both Pb and Mn reduced
brain weight to a greater extent than either metal alone [37]. Each of these studies also showed that co-exposure to Mn
and Pb led to increased brain Pb levels, perhaps because of changes in affinity of Pb-binding proteins in the brain [38].
In addition, multiplicatively greater changes in monoaminergic neurotransmitter levels occur in the brains of rats
exposed to Pb and As jointly, compared either metal aloneor to combinations of Pb, Mn, and As [39]. observed that Mn
and As had greater accumulation in rat brains relative to controls with single metal exposures [40].The 3 metal
concentrations when combined were associated decreases in dopaminergic metabolites and increases in serotinergic
metabolites. Overall, these findings are complex, but the data support the concept that co-exposure to multiple metals
may cause neurotoxic effects not seen with exposure to a single metal at the same dose [19].
Neurotoxicity of Methylmercury
Toxic effects on the brain due to methylmercury were first established in men with occupational exposure [41].The
developmental toxicity of this organic mercury compound became evident in the 1960s in Minamata, Japan, where an
epidemic of spasticity, blindness and profound mental retardation was seen in infants born to mothers who consumed
fish from contaminated waters. After many years of clinical and experimental studies, the source proved to be mercury
compounds released into Minamata Bay by a plastics plant [42].Methylmercury accumulated and reached high
concentrations in locally caught fish. Exposed adults, including mothers of poisoned children, were less seriously
affected, if at all [43].Similar outbreaks of profound neurodevelopmental disorders in the infants of seemingly
unaffected mothers have arisen after maternal consumption during pregnancy of seed grain treated with methylmercury
fungicides [44, 45].Studies of a serious poisoning incident in Iraq established a crude dose-response association
between mercury concentrations in maternal hair and risk of neurological abnormalities in the children of the women
[46].Recent studies have focused on prenatal exposures to reduced concentrations of methylmercury. They have
examined populations with a high intake of seafood and freshwater fish with various degrees of methylmercury
contamination. Prospective examination of a New Zealand cohort noted a three-point decrement in intelligence quotient
(IQ) and changes in affect in children born to women with mercury concentrations in hair of greater than 6 μg/g.40 A
large prospective study in the Faroe Islands noted evidence of dose-related impairments in memory, attention,
language, and visuospatial perception in exposed children [47].A third prospective cohort study in the Seychelles
provided no support for prenatal neurotoxicity after adjustment for postnatal exposures [48].Several cross-sectional
studies recorded significant associations between methylmercury exposure and neurobehavioral impairment in young
children [49].
Neurotoxicity of Arsenic (As)
Ingestion of arsenic-contaminated drinking water has long been recognised to cause peripheral neuropathy in adults
[50].Developmental neurotoxicity due to arsenic was reported in 1955 in Japan, where consumption of powdered milk
contaminated with arsenic led to over 12 000 cases of poisoning and 131 deaths.A follow-up study of three groups of
adolescents born during the time of the milk contamination included one group that was fully breast-fed, one that was
exposed to the tainted milk product, and one that received other supplements, but no tainted formulaCompared with
national rates, a ten-fold increase in mentally-retarded individuals was seen in the tainted milk group poor school
records, emotional disturbances, and abnormal or borderline electro-encephalogram findings were also more common
in the exposed group. Since these findings were initially reported in Japanese journals not easily available elsewhere
[51,52],they have often been overlooked, even in the most thorough risk assessments of environmental arsenic
exposure [53,54].Arsenic is present in ground water worldwide, and industrial pollution is widespread. Cross-sectional
studies of school-age children showed cognitive deficits associated with drinking water contamination52 and raised
urinary arsenic concentrations [54,55]. Similar results were obtained in children with arsenic exposure from a smelter
[56].Possible combined adverse effects on IQ caused by arsenic and manganese exposures was suggested by metal
concentrations in hair in children living near a hazardous waste site [57]. Although evidence for subclinical
neurodevelopmental neurotoxicity of arsenic is less well established than for lead and methylmercury, the data are
consistent and fit with the high-exposure findings from Japan. Still, regulatory action does not emphasize the need to
protect the developing brain against this neurotoxic substance [53,58].
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II. DISCUSSION
Heavy Metals are recognized as causes of developmental neurotoxicity. The major impact of heavy metals is on the
peoples who were directly in exposure of industries. Nowadays the major reason of nerotoxicity by which human
affected is due to toxicity from mixture of heavy metal instead of single metals. The effect of human exposure to
mixtures of heavy metals is presently anmajor research area in neurotoxicology. This proposes that contact to multiple
metals may result in higherorder of neurological effects than to single metals and this enhance need to understand the
toxicology of complex mixtures. Analysis of concentration of heavy metals in chemicals before allowing them to be
marketed is concerned to prevent toxicity, but has been seen active only in recent years.These consisted of employees
who were exposed to high doses of elements either by inhalation or accidental ingestion, and began to develop
permanent neurologic damage. Some of these information originated in industries where heavy metals exposure was
common.
III. CONCLUSION
These paper reviewed the neurotoxicity Effect of Human Health. The growing effects of Heavy metals on cognition
and behavior in children may be linked to this common theme of toxicity. The emerging brain is predominantly
sensitive to agents that disrupt synaptic activity. The practice of Heavy Metals detection should be continued to avoid
possible consumption of contaminated eatables. Neurological symptoms are recognized, early and appropriate
treatment and removal from exposure is provided, neuro toxicological and or psychological function can remain steady
or actually improve despite the earlier exposures. This is mostly prominent with peripheral neurotoxicity.
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... The clinical picture of such toxic polyneuropathies usually matches a sensoro-motor pattern with paresthesias, and in some cases weakness of the distal muscles, e.g. length-dependent neuropathy with predominant sensory symptoms [1][2][3][4]. Acute onset is rare, but possible [5]. Arsenic polyneuropathy is mainly characterized by axonal damage to sensory nerves [6] and is found in above 95% of patients. ...
... Cadmium is a known, potent toxin for cortical neurons, even in low doses [44]. Cadmium intoxication can lead to olfactory, neurobehavioral, and memory problems, and may underlie neurodegeneration [4,13,[45][46][47]. Little is known about the influence of cadmium on the peripheral nervous system [15,48]. ...
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Background Chronic exposure to heavy metals affects various organs, among them the brain and peripheral nerves. Polyneuropathy is mainly length-dependent with predominantly sensory symptoms. There have been few studies on small fiber neuropathy due to heavy metal intoxication. Methods We investigated 41 metal industry workers, mean age 51.3 ± 10.5 years, with at least 5 years’ professional exposure to heavy metals, and 36 age- and sex-matched healthy controls. We performed neurological examinations, and assessed blood levels of cadmium, lead, and zinc protoporphyrin, urine levels of arsenic, standard, sensory and motor electrophysiological tests in the ulnar and peroneal nerves, sympathetic skin responses from the palm and foot, and quantitative sensation testing from dermatomes C8 and S1. Discussion The results of standard conduction tests of all nerves significantly differed between groups. The latency of sympathetic skin responses achieved from the foot was also statistically significantly prolonged in the study group. Significant differences were seen in both C8 and S1 regions for temperature and pain thresholds, and for vibratory threshold only in the S1 region, while the dispersions of low and high temperatures were important exclusively in the C8 region. Conclusions We can conclude that co-exposure to many heavy metals results in explicit impairment of peripheral nerves. The lesion is more pronounced within small fibers and is predominantly connected with greater impairment of temperature-dependent pain thresholds. The evaluation of small fiber function should be considered in the early diagnosis of toxic polyneuropathy or in low-dose exposure to heavy metals.
... Among heavy metals, cadmium, lead, arsenic, zinc, and nickel are of special importance due to their long half-lives in humans and other animals and their high toxicity (Jaishankar et al., 2014, Yüksel et al., 2021. Because of the carcinogenic and neurotoxic effects of heavy metals, even in very small quantities, special attention has been paid to this issue worldwide (Sankhla et al., 2017). In recent years, new analytical methods for measuring and analyzing metal content (even at ppb levels) have been able to search for disorders related to the consumption of heavy metals and then examine the carcinogenic effects on various organs (El-Moselhy et al., 2014). ...
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The present paper assesses human health risk associated with accumulation of lead, copper, zinc, nickel, and Arsenic in the muscle of bartail flathead (Platycephalus indicus) collected from Jofreh Pier and Bushehr Port, northwest of the Persian Gulf of Iran. It collects eighty P. indicus in total, analyzing them via ICP-OES of two seasons (summer and winter) of 2019. Thus, it manages to estimate daily intake (EDI), estimated weekly intake (EWI), target hazard quotient (THQ), hazard index (HI), and Carcinogenic risk (CR). The mean concentration (μg/g) range are observed as follows: zinc (16.37-50.17)> As (5.65-8.83)> Cu (2.19-3.63)> Pb (0.62-6.37)> Ni (0.17-1.08). Hazard index (HI) for adult and children during consumption of P.indicus has been below 1, with the highest HI values calculated for adults (0.06) in Bushehr and children (0.14) in Jofreh. The CR levels for Ni and Pb have been within acceptable limits (10-6 to 10-4), while arsenic has stood at unacceptable levels (> 10-4) in the sampling sites.
... OS is the condition of abnormal production of free radicals or oxidants and altered antioxidant status. HM-induced OS targets biomolecules such as antioxidant enzymes, proteins, lipids, and DNA can be carcinogenic (Zefferino et al. 2017;Zafarzadeh et al. 2018;Duan et al. 2020) as well as neurotoxic (Sankhla et al. 2017;Branca et al. 2018;Anyanwu et al. 2020). ...
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Heavy metal-induced toxicity contributes to the progression of various metabolic disorders and possible mechanisms involved in disease progression are not well established. In this study, the correlation of heavy metal exposure and hypertension have been demonstrated. The results showed that in hypertensive subjects, the lipid profiles (triglycerides, LDL-C, HDL-C, and total cholesterol) and cardiac markers (CK-MB and LDH) were altered abruptly. As a consequence of heavy- induced oxidative stress, the oxidants (TBARS and protein carbonyls) and antioxidants (SOD, GSH, and TAC) were significantly increased and decreased, respectively in hypertension subjects. The concentrations of heavy metals (Pb, Cd, and As) exceeded the permissible limits in hypertensive subjects. The Nrf-2 genotyping indicated that heavy metals may induce mutations at molecular level. The results of correlation analysis revealed that the heavy metals interact with cellular components and interfere with metabolic processes which then results in disturbed lipid profile, enhanced oxidative stress, and reduced antioxidant status. The current study systematically estimated the association of hair and nail heavy metal concentrations with hypertension among the population residing in the Malwa region of Punjab. The proposed study highlighted that heavy metals act as a silent risk factor in the hypertension progression in the population of Malwa region. Future studies are required to confirm current findings and further scrutinize the effect of heavy metals exposure in early adulthood, early, and late mid-life to develop metabolic complications such as hypertension.
... The hazard of biomagnification and bioaccumulation of the Ni and Zn causes extreme harm to human health and welfare. Industrial effluent is one of the prime sources of metal [5][6][7][8][9][10][11][12][13] contamination in river waters is no exception . Although Zinc is an essential element for a healthy body, excessive zinc can be extremely toxic to human health. ...
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Introduction: Yamuna river is the longest and second-largest tributary of the Ganga river. The tenacious river pollution concentrations of Nickel and Zinc were determined in water from river Yamuna, at Delhi. The polluted river water is mostly used for drinking, agricultural or aquacultural purposes and also stored as holy water. Due to growing community extension, farm and residential advancement and rapid technological progress are significant origins of the decay of lead in Yamuna river and various water sources. Material & Method: The objective of this study was to determine the seasonal variation of Nickel and Zinc concentration in Yamuna river water from summer, monsoon and winter and water samples were collected from five different sites of the river. The seasonal variation of metal concentration is determined using Inductively Coupled Plasma Mass Spectrometry (ICP-MS) & Atomic Absorption Spectroscopy (AAS). Result: The Ni and Zn concentrations in Yamuna river water are higher than the limits of WHO set for heavy metals. The highest concentration of Ni and Zn metals in river water are found in the summer season. It is universally-known that the Ni and Zn are majorly toxic in nature. The exposure of the Ni and Zn through water is chronic toxicity, which could be quite harmful to humans as well as underwater life. Conclusion: This research study shows that the water quality of the Yamuna river is not fit for drinking, bathing, agricultural purpose and aquatic life. The existing condition of the Yamuna river is of serious concern, and remediation of the river to prevent current and further pollution is the critical need for environmental conservation.
... The thio groups are the most prevalent functional groups that heavy metals fixes to (SH group of cysteine and SCH3 group of methionine). Cadmium had shown to bind to cysteine remains in the catalytic surface of human thiol transfers in vitro, consisting thioredoxin reductase, glutathione reductase, as well as thioredoxin [65][66][67][68][69][70]. ...
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Vegetables are a prevalent nutrition for people all over the world because they are high in important nutrients, antioxidants, and metabolites that function as buffers for acidic compounds created during digestion. Vegetables, on the other hand, absorbed both vital and poisonous substances through the soil. Possible human health concerns, including as cancer and renal damage, have been linked to the consumption of heavy metal-contaminated vegetables (HMs). Heavy metals like Cr, Mn, Fe, Ni, Cu, Zn, Cd, Pb, and Hg were found in high concentrations in popular vegetables such as Amaranthus tricolour L., Chenopodium album L., Spinacia oleracea, Coriandrum sativum, Solanum lycopersicum, and Solanum melongena. The toxicity, fortification, health hazard, and heavy metals sources grown in soil are detailed in this review study.
... Lead is a toxic heavy metal in different sources such as contaminated drinking water, battery manufacture, cosmetics, leaded gasoline, lead-based paint, cans, glazed ceramics, traditional herbal medicine products, water pipes, jewelry, tobacco smoke, and electronic cigarettes, and toys. Lead exposure can be considered a public health concern, especially in early childhood, because children have increased hand-to-mouth activity, so they are more at risk [13,14]. While the half-life of Pb in the bloodstream is about 35 days, it is stored in bones for approximately 30 years [15,16]. ...
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Neurotoxicity may develop with exposure to various substances such as antibiotics, chemotherapeutics, heavy metals, and solvents. Some plants and fungi are also known to be neurotoxic. Neurotoxicity can develop acutely within hours, or it can develop as a result of exposure for years. Neurotoxicity can be presented with central or peripheral nervous system findings such as neurobehavioral symptoms, extrapyramidal signs, peripheral neuropathy. Peripheral nerve fibers are affected in different ways by neurotoxicant injury. The pattern of injury depends on the target structure involved. The focus of this chapter includes signs, symptoms, pathophysiology, and treatment options of neurotoxicity.
... Last, this study included a limited number of metals. Although those metals were major neurotoxicants, other neurotoxic metal such as arsenic (Freire et al., 2018), iron (Tamura et al., 2002), zinc (Sankhla et al., 2017), and copper (Prohaska, 2000), were not included. ...
Article
Background Humans are exposed to a mixture of metals during their lifetime; however, evidence of neurotoxicity of such mixtures in critical time windows is still insufficient. We aimed to elucidate the associations of four metals mixture across multiple time points with children’s intelligence quotient (IQ) in a prospective cohort study. Methods Prenatal exposure and exposure at age 4 and 6 years to four types of blood metals, namely lead, mercury, cadmium, and manganese were quantified in 502 pregnant women and their children who participated in the Environment and Development Cohort study. Children’ s IQ scores were assessed using the Wechsler Intelligence Scale at age 6. Bayesian kernel machine regression (BKMR), quantile g-computation models, and elastic net (ENET) models were used to assess the associations of their blood metals mixture with IQ scores. Results Multivariate linear regression models indicated that postnatal blood manganese exposure at the age of 4 years was significantly negatively associated with children’s IQ [β = − 5.99, 95% confidence interval (CI): −11.37 to − 0.61]. In the multi-chemical BKMR and quantile g-computation model, statistically significant inverse associations were found between the mixture of prenatal and postnatal metals and children’s IQ score (Difference in children’ IQ per quartile increase: −2.83; 95% CI: −5.28, −0.38). Interestingly, we found that manganese levels at both age of 4 and 6 years were contributing factors to children’s IQ in the mixture models, namely, BKMR, quantile g-computation, and ENET models. Conclusions Multi-pollutant mixtures of prenatal and postnatal exposures to four metals affected child IQ at 6 years of age. We found a relationship between manganese exposure at both age 4, and 6 years and children’s IQ. Additional studies are warranted to confirm these associations and to control the exposure to different metals during pregnancy and preschool childhood.
... Elements such as arsenic, lead, cadmium chromium, cobalt, nickel, and silica have been linked to human illnesses, including cardiovascular diseases, immune system suppression, lung injury, cancer, renal damage, neurotoxicity, and silicosis [33][34][35][36][37][38][39][40][41][42]. The metals in EC products have not yet been directly linked to these illnesses, and such linkage may be challenging to demonstrate given the high variability in metal transfer to EC aerosols from different products and the variations in user topography [43], which also affects metal concentrations in aerosols [44]. ...
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Background The atomizers of electronic cigarettes (ECs) contain metals that transfer to the aerosol upon heating and may present health hazards. This study analyzed 4 th -generation EC pod atomizer design features and characterized their elemental/metal composition. Methods Eleven EC pods from six brands/manufacturers were purchased at local shops and online. Pods were dissected and imaged using a Canon EOS Rebel SL2 camera. Elemental analysis and mapping of atomizer components was done using a scanning electron microscope coupled with an energy dispersive x-ray spectrometer. Results EC pods varied in size and design. The internal atomizer components were similar across brands except for variations occurring mainly in the wicks and filaments of some products. The filaments were either Elinvar (nickel, iron, and chromium) (36.4%), nichrome (36.4%), iron-chromium (18.2%), or nickel (9%). Thick wires present in 55% of the atomizers were mainly nickel and were joined to filaments by brazing. Wire-connector joints were Elinvar. Metal air tubes were made of Elinvar (50%), nickel, zinc, copper, and tin (37.5%), and nickel and copper (12.5%). Most of the wick components were silica, except for two pods (PHIX and Mico), which were mainly ceramic. Connectors contained gold-plated nickel, iron-chromium multiple alloys of nickel, zinc, gold, iron, and copper. Wick chambers were made of Elinvar. Outer casings were either nickel, copper-tin, or nickel-copper alloys. Magnets were nickel with minor iron, copper, and sulfur. Some frequently occurring elements were high in relative abundance in atomizer components. Conclusions The atomizers of pods are similar to previous generations, with the introduction of ceramic wicks and magnets in the newer generations. The elements in EC atomizers may transfer into aerosols and adversely affect health and accumulate in the environment.
Article
Honey may have potential benefits due to its nutrient and bioactive molecules. On the other hand, it is a food that could be affected by environmental pollution; therefore, honey may contain contaminants such as heavy metals. The present study aimed to quantify eleven heavy metals and essential elements (Hg, Cd, V, Cr, Ni, Cu, As, Sb, Pb, Ba, Mn) in honey collected in the Campania region (Italy) and analyzed through Q-ICP-MS. Secondly, carcinogenic and non-carcinogenic risks due to ingestion of honey in toddlers, adolescents, and adults were estimated based on the Target Hazard Quotient (THQ) and Lifetime Cancer Risk (LTCR). No statistically significant difference emerged among the different areas. The risk assessment did not report concerns for non-carcinogenic risk. However, the three groups showed a potential carcinogenic risk for Ni, Cr, and As, even though toddlers reported higher exposure values. The finding of this study provides pieces of knowledge on levels of contaminants in honey in Campania. Furthermore, it can aid in understanding the resulting risk due to honey ingestion.
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Heavy metals accumulated the earth crust and causes extreme pollution. Accumulation of rich concentrations of heavy metals in environments can cause various human diseases which risks health and high ecological issues. Mercury, arsenic, lead, silver, cadmium, chromium, etc. are some heavy metals harmful to organisms at even very low concentration. Heavy metal pollution is increasing day by day due to industrialization, urbanization, mining, volcanic eruptions, weathering of rocks, etc. Different microbial strains have developed very efficient and unique mechanisms for tolerating heavy metals in polluted sites with eco-friendly techniques. Heavy metals are group of metals with density more than 5 g/cm3. Microorganisms are generally present in contaminated sites of heavy metals and they develop new strategies which are metabolism dependent or independent to tackle with the adverse effects of heavy metals. Bacteria, Algae, Fungi, Cyanobacteria uses in bioremediation technique and acts a biosorbent. Removal of heavy metal from contaminated sites using microbial strains is cheaper alternative. Mostly species involved in bioremediation include Enterobacter and Pseudomonas species and some of bacillus species too in bacteria. Aspergillus and Penicillin species used in heavy metal resistance in fungi. Various species of the brown algae and Cyanobacteria shows resistance in algae.
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People relate the neural disorders with either inheritance or psychological violence but there might be some other reasons responsible for the ailment of people that do not have such a background. The present study explains the chronic effect of heavy toxic metals on nervous system. During experimentation, rabbits used as laboratory animals, were given test metals in their diet. Concentration of metals given to them in the diet was less than their tolerable dietary intake. Behavioral changes were observed during experimentation. Periodic increase in the metal concentration was seen in the blood sample of rabbits. They were slaughtered after a period of eight months of slow poisoning. Histological examination of brain tissues was performed. The brain samples were analyzed by Atomic absorption spectroscopy and Inductively Coupled Plasma Mass Spectrometry to find the retention of heavy metals in mammalian brain. Concentration of lead, mercury and cadmium in the blood samples of occupationally exposed people and patients with neurological disorders at the time of neurosurgery was determined by using the same techniques. During circulation, toxic metals passes through the nerve capillaries to settle down in the brain. Heavy metals cross the blood brain barrier and 'may retain themselves in it. Brain tumors and biopsy samples of patients with neurological disorder were also analyzed to relate neurotoxicity and heavy metal poisoning. Results obtained shows that lead, mercury and cadmium retain themselves in the brain for longer period of time and are one of the causes of neurotoxicity.
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Present study is an attempt to evaluate feces as bioindicator of heavy metal contamination in captive zoo mammals. This is a non-invasive technique to study gross exposure of metal pollution. Various metal contents in mammals of Bikaner (India) zoo were in the range of 58.4±3.14 (Cervus unicolor) to 1.82±0.96 (Panthera. tigris) ppm d/w. Cadmium was in range between 2.46±0.08 (Axis axis) to 0.41±0.03 (Macaca mulatta) ppm d/w. Chromium was in rage of 91.68±2.28 (Oryctolagus cuniculus) to 1.36± 0.36(Macaca mulatta) ppm d/w. Copper was in range between 22.82±2.18 (Panthera pardus) to 6.15±0.45 (Boselaphus tragocamelus). Whereas zinc was found in range of 35.6±1.35 (Canis aureus) to 8.15±0.45 (Boselaphus tragocamelus) ppm d/w. Analysis of feed and water along with the soil in cages which is receiving particulate air pollutants indicates that air pollution is the primary cause due to high density of traffic in the area.
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Mercury pollution in different regions of the world is a growing concern from an environmental and epidemiological point of view. The increasing trends of energy production from fossil fuel combustion, mercury usage in a large variety of goods and products, and the lack of emission control policy, especially in fast developing countries, represent a major environmental and political issue for national and international organisations and governments as well. In the last decade, there has been a significant effort to improve our knowledge on different aspects involved in the biogeochemical cycle of mercury in the environment and its impact on human health. Special attention has been devoted to fill the gaps in our knowledge on physical and chemical processes involved in the transfer of mercury compounds released to the atmosphere from natural and anthropogenic sources to terrestrial and aquatic receptors. Significant progress was made on assessing the spatial and temporal distributions of atmospheric mercury and its depositional fluxes. Dynamics of Mercury Pollution on Regional and Global Scales: Atmospheric Processes and Human Exposures Around the World provides a detailed overview of our current understanding of different dynamic patterns involved in the redistribution of mercury in the global environment, and its impact on human health and ecosystems. © 2005 Springer Science+Business Media, Inc. All rights reserved.
Article
In 1955, many babies who had drunk arsenic-tainted milk produced at the Tokushima Plant of the Morinaga Milk-Industry Company Ltd., suffered from serious poisoning. The number of victims ascertained in February, 1956 covering 27 prefectures in the western part of Japan was 12, 159, of whom 131 died.The disaster was caused by the process of manufacturing the powdered milk. Disodium phosphate was added as a stabilizer to make the milk easily soluble. This disodium phosphate was poorly purified, intended for non-food industrial use, and contained a toxic dose of arsenic, sodium arsenite and vanadium compounds etc.Shortly after the disaster, numerous medical reports were published. A committee organized by the Society for Child Health (the chairman was Prof. Nishizawa of Osaka University; so it was called the Nishizawa Committee), determined criteria for the diagnosis of the poisoning; but these criteria were inadequate and erroneous from several points of view. Strange to say, debates and publications about the disaster disappeared quickly after the report was published by the Health Department of Okayama Prefecture stating that the victims had recovered completely according to the criteria established by the Nishizawa Committee only one year after the disaster.Until 1969, when Prof. Maruyama et al., of Osaka University reported on victims whom they had visited, no study had been made to ascertain whether or not there were any after-effects of the poisoning. Much fault must be found with the Ministry of Health and Welfare, with the attitude of the Morinaga Company, and with the doctors concerned, for this neglect to follow-up such an unprecedented and large-scale disaster.In 1969, the authors managed to organize an epidemiological study group with several departments of Hiroshima University and the Department of Hygiene of Okayama University cooperating and have developed joint research on this disaster as follows:1. A follow-up survey was made among victims in Okayama Prefecture between December 1969 and April 1970. 214 people answered the questionnaire and 74 were given a medical examination.2. A prospective study was made on the basis of a questionnaire on clnical complaints collected at the time of the disaster in 1955.3. A comparative study was performed between the victims and their brothers and sisters.4. A comparative study was performed among handicapped children in institutions in Okayama Prefecture, who were born between January 1st, 1953 and December 31st, 1955. The children were divided into three groups, namely those who had consumed the arsenic-tainted milk, those who were brought up on different brands of powdered milk from different companies, and those fed only maternal milk.5. A comparative study was performed among all children born between January 1st, 1954 and December 31st, 1955 and brought up in Seno district in Hiroshima Prefecture which has a relatively stationary population and where good records had been kept of the physical growth and mental development of the children in the nursery, primary and junior high schools. The children were divided into the same three groups as mentioned above. This study was performed as a joint research project by the Departments of Public Health (Director: Prof. M. Tanaka), Orthopedics (Director: Prof. K. Tsuge), Ophthalmology (Director: Prof. T. Dodo) and Psychiatry and Neurology (Director: Prof. K. Sarai) of Hiroshima University Medical School and Deparment of Conservative Dentistry (Director: Prof. T. Inoue) of Hiroshima University Dental School, and Department of Hygiene (Director: Prof. M. Ohira) of Okayama University Medical School. All clinical examinations were conducted separately under the double blind method.6. The 124 cases of the children examined in the district of Senogawa town were discussed individually by the six medical doctors and five dentists who did the examinations.
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Approximately 1.5 million workers in the United States are exposed to arsenic. Occupational exposure is primarily by inhalation. NIOSH recommends that time-integrated exposure to arsenic in air not exceed 2 μ.g/m3. Recent exposure is accurately measured by urine assay; urine arsenic concentrations above 50 μg/liter indicate increased absorption. Hair assay is a semiquantitative index of past exposure. Toxicity is associated primarily with the trivalent (3 + ) form of arsenic. Acute poisoning is caused most commonly by contaminated food or drink; it is rarely occupational. Chronic intoxication is characterized by dermatitis, hyper-pigmentation, keratoses, peripheral neuropathy (primarily sensory), irritation of the upper and lower respiratory tract, and occasionally by hepatic toxicity and peripheral vasculopathy (blackfoot disease). Arsenic is not carcinogenic in animal species, but is mutagenic in Syrian hamster cells. In man, arsenic is known definitely to cause cancer of skin, lung, and liver (angiosarcoma) and possibly to cause lymphoma.