Occupational arsenic exposure and glycosylated haemoglobin†

Abstract

In a group of 40 workers occupationally exposed to arsenic (As workers) biological markers for cardiovascular diseases were studied. The median arsenic concentration in urine samples from the exposed group was 22.3 nmol of As per mmol of creatinine, while the individual maximum level was 294.5 nmol of As per mmol of creatinine. That of the reference group was 12 nmol of As per mmol of creatinine and significantly below the level of the exposed group (p < 0.001). The arsenic concentration in urine samples from colleagues of the persons working with arsenic containing products was similar to the arsenic concentration in urine samples from the As workers. The concentration of glycosylated haemoglobin (Hgb A1C) was increased in whole blood from the As workers. The level of the As workers was 5.4% (median), similar to that of colleagues (5.5%), while that of the reference group was 4.4%. The differences were significant (p < 0.001). Multiple regression analysis showed a significant connection (p = 0.034) between the concentration of Hgb A1C in whole blood and the arsenic level in urine from the As workers. The systolic blood pressure was 125 mm Hg in the As workers and 117 mm Hg in the control group. The difference was significant (p = 0.023). It is concluded that arsenic exposure has an influence on carbohydrate metabolism, increases the systolic blood pressure and finally may result in increased risk of development of cardiovascular diseases.

Examination of the effects of arsenic on glucose homeostasis in cell culture and animal studies: Development of a mouse model for arsenic-induced diabetes

“…The link between diabetes mellitus and consumption of water containing iAs was later confirmed by several cross-sectional and cohort studies from Taiwan (Tseng et al, 2000) and Bangladesh (Rahman et al, 1998;Rahman et al, 1999). Other studies have examined the association between exposure to iAs in occupational settings and the occurrence of symptoms that are consistent with diabetes (Jensen and Hansen, 1998;Rahman and Axelson, 1995;Rahman et al, 1996). These studies were retrospective in nature and primarily used death certificates as their diagnostic criteria.…”

A review on exposure and effects of arsenic in passerine birds

“…Increased incidences of Raynaud's phenomenon (peripheral vascular disease), vasospasticity, increased systolic blood pressure Humans Jensen and Hansen (1998); Lagerkvist et al (1986) Dermal effects Dermatitis, mild pigmentation, keratosis of skin, or gross pigmentation with hyperkeratinization of exposed skin Humans Cöl et al (1999); Perry et al (1948) Neurological effects Increased in peripheral neuropathy, decreased nerve conduction velocity Humans Feldman et al (1979); Lagerkvist and Zetterlund (1994) Developmental effects Increased incidence of abortion and congenital malformations in children Humans Nordström et al, (1979aNordström et al, ( , 1979b Ocular effects Chemical conjunctivitis Humans Pinto and Mcgill (1953) Cancer Lung cancer Humans Enterline et al, (1987aEnterline et al, ( , 1987b Holson et al (1999); Nagymajtényi et al (1985) Immunological effects Decreased pulmonary bactericidal activity and increased susceptibility to streptococcal infections Mouse Aranyi et al (1985) Gastrointestinal effects Gross gastrointestinal lesions Rat Holson et al (1999) Inhalation exposure (organic arsenic) Respiratory effects Respiratory distress and bright red lungs with dark spots Rat and mouse Stevens et al (1979) Dermal effects Erythematous lesions on feet and ears (probably due to direct irritation from dermal contact with the dust) Rat Stevens et al (1979) Ocular effects Encrustation around the eyes (probably due to direct irritation from ocular contact with the dust)…”

Molecular and ionic mimicry and the transport of toxic metals

“…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).…”