Carbon monoxide, carbon disulfide, lead and cadmium — Four examples of occupational toxic agents linked to cardiovascular disease

Wojtczak-Jaroszowa, J; Kubow, Stan

doi:10.1016/0306-9877(89)90101-1

Cited by 24 publications

(13 citation statements)

References 88 publications

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“…For example, in patients exposed to lead, decreases in total cholesterol and the low-density lipoprotein (LDL) fraction together with an increase in the high-density lipoprotein (HDL) fraction are described (Cocco et al 1991). The other mechanism postulated to accelerate lead-induced atherosclerosis is stimulation of lipid peroxidation, causing damage to vessel endothelium and increasing the tendency to blood clotting (Quinlan et al 1988;Wojtczak-Jaroszowa and Kubow 1989;Xiao et al 1989).…”

Section: Introductionmentioning

confidence: 98%

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Lipid abnormalities in rats given small doses of lead

1993

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Previous human and experimental studies have demonstrated that lead exposure may modify the metabolism of lipids. Several studies have indicated that exposure to lead produces an increase in lipid peroxidation and inhibits blood superoxide dismutase activity. Recently, lipid peroxides have been shown to impair tissue membranes and to be a risk factor for vascular diseases. The aim of the present investigation was to evaluate the impact of subclinical lead poisoning on rat lipids in the context of atherosclerosis. The degree of poisoning was analogous to that in populations exposed to lead in a contaminated environment. Experiments were performed on male Buffalo rats with body weights of 150-200 g. The experimental animals received lead acetate intragastrically in doses of 35 mg lead/kg body wt. (Pb/kg) once weekly or 70 mg Pb/kg twice weekly for 7 weeks. Control rats were fed in the same manner with sodium acetate equimolar to the acetate in the lead acetate solution. One day after the feeding was over, venous blood samples, under ether anesthesia, were collected. The animals were killed by exsanguination and the liver was excised for determination of the metal (lead, copper, and zinc) content. A segment of the abdominal aorta was excised for histological examination. In venous blood the following were estimated: triglycerides, total cholesterol, high-density lipoprotein (HDL)-cholesterol fraction, serum lipid peroxides, and blood superoxide dismutase activity. Metal content (lead, copper, and zinc) in blood and liver was determined by means of atomic absorption spectrophotometry. In rats poisoned with small doses of lead, decreases in the plasma cholesterol level and the HDL-cholesterol fraction were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Introductionmentioning

confidence: 98%

“…The postulated mechanisms include an increase in blood cholesterol levels and/or induction of lipid accumulation in vessel walls (Kopp et al 1988;Wojtczak-Jaroszowa and Kubow 1989). However, the significance of the atherogenic effect of lead remains to be better understood.…”

Section: Introductionmentioning

confidence: 99%

Lipid abnormalities in rats given small doses of lead

1993

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“…Several reports have shown that both acute and chronic lead poisoning cause impairment of heart and vessel function5 6 and that rates of death from cerebrovascular disease are significantly increased in lead-exposed workers compared with the general population.9 However, no clear data are available demonstrating a higher mortality rate from heart disease in subjects exposed to lead. 1 An association between atherosclerosis and lead exposure is biologically plausible.…”

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confidence: 99%

“…Microscopic analysis of lead-intoxicated animals has indicated fatty degeneration of the myocardium and sclerotic changes in the aorta and walls of the small arteries, especially the renal, cerebral, and coronary arteries,11-4 and atrophy of elastic fibers in the aorta.15 Thus, it has been suggested that one ofthe underlying mechanisms in the association between cardiovascular damage and lead exposure is the induction or acceleration of atherosclerosis. 6 According to Wojtczak-Jaroszowa and …”

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confidence: 99%

The association between occupational lead exposure and serum cholesterol and lipoprotein levels.

Kristal-Boneh¹,

Coller²,

Froom³

et al. 1999

Am J Public Health

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OBJECTIVES: This study sought to clarify the possible associations between blood lead level and serum cholesterol and lipoprotein levels in subjects occupationally exposed to lead. METHODS: Levels of blood lead, serum total cholesterol, high-density lipoprotein (HDL) cholesterol, low-density lipoprotein cholesterol, and triglycerides in 56 male industrial employees who were exposed to lead were compared with those in 87 unexposed employees. RESULTS: Mean blood lead levels were 42.3 (+/- 14.9) micrograms/dL in the exposed group and 2.7 (+/- 3.6) micrograms/dL in the nonexposed group. The exposed subjects had higher mean levels of total cholesterol and HDL cholesterol. CONCLUSIONS: Blood lead levels are positively associated with total and HDL cholesterol.

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“…Thus, the reduced rCBF in the brain CT perfusion scan might represent a microangiopathy, which may subsequently induce central demyelination in the brain MRI. Clinical and experimental studies have shown that CS 2 exposure may accelerate atherosclerosis, particularly of the aorta, and the cerebral, renal and coronary arteries [3, 9, 10, 24, 25, 26, 27]. In addition, demyelination changes have been found in the globus pallidus, and perivascular demyelination has been observed in the subcortical areas in some experimental animals [3, 22, 28].…”

Section: Discussionmentioning

confidence: 99%

Diffuse White Matter Lesions in Carbon Disulfide Intoxication: Microangiopathy or Demyelination

Huang

Kuo

et al. 2003

Eur Neurol

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Long-term exposure to carbon disulfide (CS₂) may induce diffuse encephalopathy with parkinsonism, pyramidal signs, cerebellar ataxia, and cognitive impairments, as well as axonal polyneuropathy. The pathogenic mechanisms of diffuse encephalopathy are unclear, although vasculopathy and toxic demyelination have been proposed. Recently, we have encountered a patient who developed headache, limb tremors, gait disturbance, dysarthria, memory impairment, and emotional lability after long-term exposure to CS₂. The brain magnetic resonance images (MRI) showed diffuse hyperintensity lesions in T₂-weighted images in the subcortical white matter, basal ganglia, and brain stem. The brain computed tomography perfusion study revealed a diffusely decreased regional cerebral blood flow and prolonged regional mean transit time in the subcortical white matter and basal ganglion. To our knowledge, there have been few reports demonstrating diffuse white matter lesions in chronic CS₂ encephalopathy using brain MRI. In addition, the ^99mTc-TRODAT-1 single photon emission computed tomography showed a normal uptake of the dopamine transporter, indicating a normal presynaptic dopaminergic pathway. We conclude that diffuse white matter lesions may develop after chronic exposure to CS₂, possibly through microangiopathy. In addition, CS₂ poisoning can be considered as one of the causes of chronic leukoencephalopathy.

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Carbon monoxide, carbon disulfide, lead and cadmium — Four examples of occupational toxic agents linked to cardiovascular disease

Cited by 24 publications

References 88 publications

Lipid abnormalities in rats given small doses of lead

Lipid abnormalities in rats given small doses of lead

The association between occupational lead exposure and serum cholesterol and lipoprotein levels.

Diffuse White Matter Lesions in Carbon Disulfide Intoxication: Microangiopathy or Demyelination

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