Assessment of exposure to arsenic among smelter workers: A five‐year follow‐up

Lagerkvist, Bengt; Zetterlund, Bo

doi:10.1002/ajim.4700250403

Cited by 69 publications

(32 citation statements)

References 20 publications

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“…Numerous studies have shown that this metal has deleterious effects on the respiratory (Civantos et al, 1995;Dunlap, 1921;Lundgren, 1954;Morton and Caron, 1989;Pinto and McGill, 1953;Sandstrom et al, 1989), neurological (Armstrong et al, 1984;Blom et al, 1985;Civantos et al, 1995;Feldman et al, 1979;Lagerkvist and Zetterlund, 1994), and cardiovascular (Cullen et al, 1995;Jensen and Hansen, 1998;Lagerkvist et al, 1986Lagerkvist et al, , 1988 systems. The most common and well-characterized sign of As poisoning is the development of skin lesions and warts (Bickley and Papa, 1989;Dunlap, 1921;Holmqvist, 1951;Lagerkvist et al, 1986;Mohamed, 1998;Perry et al, 1948;Pinto and McGill, 1953).…”

Section: Arsenicmentioning

confidence: 99%

Molecular and ionic mimicry and the transport of toxic metals

Bridges

Zalups

2005

Toxicology and Applied Pharmacology

677

460

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Despite many scientific advances, human exposure to, and intoxication by, toxic metal species continues to occur. Surprisingly, little is understood about the mechanisms by which certain metals and metal-containing species gain entry into target cells. Since there do not appear to be transporters designed specifically for the entry of most toxic metal species into mammalian cells, it has been postulated that some of these metals gain entry into target cells, through the mechanisms of ionic and/or molecular mimicry, at the site of transporters of essential elements and/or molecules. The primary purpose of this review is to discuss the transport of selective toxic metals in target organs and provide evidence supporting a role of ionic and/or molecular mimicry. In the context of this review, molecular mimicry refers to the ability of a metal ion to bond to an endogenous organic molecule to form an organic metal species that acts as a functional or structural mimic of essential molecules at the sites of transporters of those molecules. Ionic mimicry refers to the ability of a cationic form of a toxic metal to mimic an essential element or cationic species of an element at the site of a transporter of that element. Molecular and ionic mimics can also be sub-classified as structural or functional mimics. This review will present the established and putative roles of molecular and ionic mimicry in the transport of mercury, cadmium, lead, arsenic, selenium, and selected oxyanions in target organs and tissues.

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Section: Arsenicmentioning

confidence: 99%

Molecular and ionic mimicry and the transport of toxic metals

Bridges

Zalups

2005

Toxicology and Applied Pharmacology

677

460

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“…Chronic exposure to As is associated with many negative health effects, including the development of noncancerous skin lesions (5), neuropathy (6,7), peripheral vascular diseases (8), skin (9,10), bladder (11), and lung cancers (12).…”

Section: Introductionmentioning

confidence: 99%

Toenail Arsenic Concentrations, GSTT1 Gene Polymorphisms, and Arsenic Exposure from Drinking Water

Kile¹,

Houseman²,

Rodrigues

et al. 2005

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Toenail arsenic (As) concentrations were evaluated as a biomarker of inorganic As (As in ) exposure in a population residing in an As-endemic region of Bangladesh. Drinking water and toenail samples were collected from 48 families (n = 223) every 3 months for 2 years and analyzed for As using inductively coupled plasma-mass spectrometry. Drinking water collected 3, 6, and 9 months before each toenail sample collection was combined into a weighted lagged exposure variable. The contribution of each water sample to the measured toenail As concentration was estimated using maximum likelihood that accounted for fluctuations in drinking water exposure and toenail growth. The best model attributed 69%, 14%, and 17% of the toenail As content to drinking water exposures that occurred 3, 6, and 9 months before toenail collection [95% confidence intervals (95% CI), 0.46-0.97, 0.00-0.31, and 0.03-0.35, respectively]. Generalized additive mixed models using penalized regression splines were employed to model the data. Below a drinking water concentration of 2 Mg As/L, no relationship between drinking water As and toenail As concentrations was observed. Above this concentration, toenail As content increased in a dosedependent fashion as drinking water As increased. Age was a significant effect modifier of drinking water As exposure on toenail As (b = 0.01; 95% CI, 0.002-0.02). Individuals possessing GSTT1-null genotypes had significantly more As in their toenails in contrast to GSTT1 wild-type individuals (b = 0.11; 95% CI, 0.06-0.2). Therefore, it seems that GSTT1 modifies the relationship between As in exposure and toenail As in content.

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“…Symptoms, such as myospasm, pain in the lower extremities and paresthesia were significantly related with the duration of exposure to As and its inorganic compounds. Lagerkvist and Zetterland emphasized the evident effect of exposure duration on PNS functions [6]. Reported complaints and so called mini-symptoms with concurrent abnormalities in the ENeG test may indicate subclinical neuropathy or early phase of this syndrome [14].…”

Section: Discussionmentioning

confidence: 99%

“…The reports on toxic effects of inorganic As on nervous system (NS) concern mostly workers involved in the process of copper ore refining in nonferrous metal industries. Clinical and neurophysiological studies in the copper-mill workers were carried out by Blom et al [5] and Lagerkvist and Zetterland [6]. The study groups were exposed to ambient air levels of arsenic changing over time.…”

Section: Introductionmentioning

confidence: 99%

“…Electroneurographic (ENeG) tests showed the slowing down of both motor and sensory peripheral nerve conduction velocity (NCV). Based on long-term observations, various authors emphasize that the PNS function is evidently influenced by the duration of exposure to As and its compounds [6]. Difficulties in assessing the nervous system status arise from the problems encountered in estimating exposure levels and possible combined exposure to arsenic and other metals, such as lead (Pb), copper (Cu) and zinc (Zn) occurring in copper smelting factories [8,9].…”

Section: Introductionmentioning

confidence: 99%

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Neurological and neurophysiological examinations of workers exposed to arsenic levels exceeding hygiene standards

Sińczuk-Walczak¹,

Janasik²,

Trzcinka-Ochocka³

et al. 2014

IJOMEH

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Objectives: The assessment of the neurotoxic effect of arsenic (As) and its inorganic compounds is still the subject of interest due to a growing As application in a large array of technologies and the need to constantly verify the principles of prevention and technological parameters. The aim of this study was to determine the status of the nervous system (NS) in workers exposed to As at concentrations exceeding hygiene standards (Threshold Limit Values (TLV) -10 μg/m 3 , Biological Exposure Index (BEI) -35 μg/l) and to analyze the relationship between the NS functional state, species of As in urine and As levels in the workplace air. Material and Methods: The study group comprised 21 men (mean age: 47.43±7.59) employed in a copper smelting factory (mean duration of employment: 22.29±11.09). The control group comprised 16 men, matched by age and work shifts. Arsenic levels in the workplace air (As-A) ranged from 0.7 to 92.3 μg/m 3 ; (M = 25.18±28.83). The concentration of total arsenic in urine (As tot -U) ranged from 17.35 to 434.68 μg/l (M = 86.82±86.6). Results: Syndrome of peripheral nervous system (PNS) was manifested by extremity fatigue (28.6%), extremity pain (33.3%) and paresthesia in the lower extremities (33.3%), as well as by neuropathy-type mini-symptoms (23.8%). Electroneurographic (ENeG) tests of peroneal nerves showed significantly decreased response amplitude with normal values of motor conduction velocity (MCV). Stimulation of sural nerves revealed a significantly slowed sensory conduction velocity (SCV) and decreased sensory potential amplitude. Neurophysiological parameters and the results of biological and environmental monitoring showed a relationship between As tot , As III (trivalent arsenic), the sum of iAs (As III +As V (pentavalent arsenic))+MMA (monomethylarsonic acid) concentration in urine and As levels in the air. Conclusions: The results of the study demonstrate that occupational exposure to inorganic arsenic levels exceeding hygiene standards (TLV, BEI) generates disorders typical of peripheral neuropathy.

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Assessment of exposure to arsenic among smelter workers: A five‐year follow‐up

Cited by 69 publications

References 20 publications

Molecular and ionic mimicry and the transport of toxic metals

Molecular and ionic mimicry and the transport of toxic metals

Toenail Arsenic Concentrations, GSTT1 Gene Polymorphisms, and Arsenic Exposure from Drinking Water

Neurological and neurophysiological examinations of workers exposed to arsenic levels exceeding hygiene standards

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