Cases reported "Occupational Diseases"

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1/66. Punctate keratoderma-like lesions on the palms and soles in a patient with chloracne: a new clinical manifestation of dioxin intoxication?

    We report what we believe to be a novel skin manifestation of dioxin intoxication. A 30-year-old woman with 2,3,7, 8-tetrachlorodibenzo-p-dioxin levels of 144,000 pg g-1 blood fat presented with severe chloracne that affected the entire integument. She also exhibited acral granuloma annulare-like lesions and distal onycholysis and, at a later time point, showed signs of hypertrichosis, as well as brownish-grey hyperpigmentation of the face. In addition, she developed punctate keratoderma-like lesions on the palms and soles. These lesions were negative for human papillomavirus and histologically characterized by cone-shaped hyperkeratoses invaginating, but not penetrating, into the dermis. Squamous syringometaplasia of the eccrine glands was observed in the immediate vicinity of these lesions. Both clinically and histologically these alterations are essentially indistinguishable from what is described as keratosis punctata palmaris et plantaris (KPPP). Although a fortuitous coincidence of chloracne and KPPP cannot be formally excluded, the possibility exists that in our patient toxic levels of dioxin were causally involved in this disorder of keratinization.
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2/66. An unusual case of organophosphate intoxication of a worker in a plastic bottle recycling plant: an important reminder.

    A young man was sent to our emergency unit because he had suffered from vomiting and cold sweating for 2 days. At the time he was admitted, he had no acute abdominal pains or gastrointestinal symptoms, and a physical examination revealed nothing but a faster heart rate and moist, flushing skin. The patient had worked for 6 years at a plastic bottle-recycling factory, but none of his co-workers had the same symptoms. Nevertheless, because the plant also recycled pesticide bottles, we suspected organophosphate pesticide intoxication. The patient's plasma acetylcholinesterase level was checked, revealing 1498.6 microU/L (normal range: 2,000-5, 000) on the first day and 1,379 microU/L on the second day. Upon questioning, the patient recalled that one of his shoe soles had been damaged and that his foot had been wet from walking all day in rain collected on the factory floor on the day that his symptoms first occurred. We conducted a study in the change of preshift and postshift acetylcholinesterase levels among six of his co-workers on a rainy day. We used the Wilcoxon signed rank test to compare the preshift and postshift plasma acetylcholinesterase levels; no significant difference was revealed (p = 0.600), leaving contamination via the damaged shoe sole suspect. We reviewed the literature on organophosphate intoxication; pesticide bottle-recycling factories were reported to be at a low risk of organophosphate toxicity in the working environment. However, because the potential risk of intoxication is still present, protective equipment such as clothing, gloves, and water-proof shoes should be worn, and employees should be educated on the potential risks.
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3/66. Occupational intoxication with carbon monoxide.

    The most important safety measure for prevention of CO poisoning is the installation of automatic systems that signal high CO concentrations in the work environment. public health measures that include stringent pollution control, introduction of low-cost CO monitors, and public education aimed at the high-risk population (e.g., new workers, drivers) should decrease the number of deaths from CO poisoning and should save productive years of life. Toxicity of CO is a consequence of tissue hypoxia created by the displacement of oxygen from hemoglobin and the subsequent impairment of oxygen release to the tissues. Early symptoms of CO intoxication are insidious and can resemble other diseases; physical examination may be unremarkable. For these reasons, many cases of CO poisoning are not readily recognized.
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4/66. carbon disulfide vasculopathy: a small vessel disease.

    We present the clinical manifestations of 4 male patients with acute stroke-like symptoms and polyneuropathy after long-term exposure to carbon disulfide (CS2) in a viscose rayon plant. The ages of onset of polyneuropathy ranged from 42 to 45 years with a duration of CS2 exposure between 6 and 21 years. The ages of onset of stroke were from 42 to 48 years. The risk factors for stroke including heart disease and diabetes were denied, except for smoking in 4, hyperlipidemia in 2 and hypertension in 1. At the initial visit in 1992, only 2 patients developed sudden onset of hemiparesis suggesting a lacunar stroke before the diagnosis of CS2 intoxication. Brain computed tomography (CT) scans showed low-density lesions in the basal ganglia in 2 patients, cortical atrophy in 1 and normal in 1. Brain magnetic resonance image (MRI) study disclosed multiple lesions in the corona radiata and basal ganglia on T(2)-weighted images in 3 patients and cortical atrophy in 1. After the diagnosis, they left their jobs for a CS2-free environment, and improvement of the working conditions was noted. During 5 years follow-up period, another 2 patients also developed an acute episode of stroke with hemiparesis. Brain CT and/or MRI follow-up studies in these 2 patients revealed new lesions in the basal ganglia and corona radiata. Intriguingly, a patient with previous stroke also developed new lesions in the bilateral thalami and brainstem. Carotid Doppler scan, transcranial Doppler scan and/or cerebral angiography did not show any prominent stenosis or occlusion in the major intracranial large arteries. We conclude that encephalopathy may occur in patients after long-term CS2 exposure, probably due to impaired cerebral perfusion. The lesions tend to occur in the basal ganglia, corona radiata and even brainstem, particularly involving the small-sized vessels. In addition, the cerebral lesions may progress even after cessation of CS2 exposure. Therefore, we suggest that CS2 exposure may be a risk factor for stroke.
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5/66. Neuro-ototoxicity in andean adults with chronic lead and noise exposure.

    Brainstem auditory evoked responses and audiological thresholds were used as biomarkers for neuro-ototoxicity in adults with chronic lead (Pb) intoxication from long-term Pb exposure in ceramic-glazing work. Venous blood samples collected from 30 adults (15 men and 15 women) indicated a mean blood Pb level of 45.1 micrograms/dL (SD, 19.5; range, 11.2 to 80.0 micrograms/dL) and in excess of the world health organization health-based biological limits (men, 46.2 micrograms/dL; SD, 19.6; range, 18.3 to 80.0 micrograms/dL; women, 44.0 micrograms/dL; SD, 20.1; range, 11.2 to 74.2 micrograms/dL). Mean auditory thresholds at frequencies susceptible to ototoxicity (2.0, 3.0, 4.0, 6.0, and 8.0 kHz) revealed sensory-neural hearing loss in men, which may be attributable to occupational noise exposure in combination with Pb intoxication. Bilateral brainstem auditory evoked response tests on participants with elevated blood Pb levels (mean, 47.0 micrograms/dL) showed delayed wave latencies consistent with sensory-neural hearing impairment. The results suggest that environmental noise exposure must be considered an important factor in determining sensory-neural hearing status in occupationally Pb-exposed adults.
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6/66. Occupational absorption of tellurium: a report of two cases.

    Industrial uses of tellurium are limited, and reported cases of tellurium absorption of occupational origin are rare. Two such cases are reported here. Both showed typical signs and symptoms of intoxication; in particular, the stench of sour garlic was noted on breath and from excreta. An unusual feature was the bluish-black discoloration of the webs of the fingers and streaks on the face and neck. Full hospital investigation was negative. No permanent damage resulted and each patient made a spontaneous recovery without treatment.
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7/66. Superior vena cava thrombosis in chronic lead exposure--a case report.

    Thrombosis is a rare cause of superior vena cava syndrome (SVCS). A 43-year-old male patient with SVCS due to thrombosis underwent investigation for the etiology of thrombus formation. He had been hospitalized several times because of lead intoxication in the past. lead has a known thrombogenetic effect experimentally. This patient with superior vena cava thrombosis had thrombophilia that was probably due to lead intoxication. The etiologies of venous thrombosis and thrombogenetic effect of chronic lead exposure are discussed.
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keywords = intoxication
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8/66. An investigation of solvent-induced neuro-psychiatric disorders in spray painters.

    An index case of chronic toxic encephalopathy is described in a 28 year old male spray painter with eleven years of exposure to solvents at work. The patient had progressive affective symptoms following repeated past episodes suggestive of acute solvent intoxication. He also showed impaired performance on tests of auditory memory, perceptual speed, visual scanning, and manual dexterity, as well as electromyographic evidence of prolongation of distal terminal latency and slowing of conduction velocities. The case investigation was followed up with an epidemiological study of the factory where he worked, to determine if other spray painters might have similar excessive complaints of neuropsychiatric symptoms and/or objective neurobehavioural deficits. This involved 15 other male spray painters employed for at least five years, and a sex- and age-matched group of 15 control workers not exposed to solvents. The spray painters reported significantly more numbers of neurobehavioural symptoms than the controls. There were little differences in neurobehavioural test results, except for aiming test (psychomotor co-ordination) and Benton visual retention test (visual memory). Spray painters with four or more neurobehavioural symptoms also performed more poorly on Digit Symbol (perceptual speed) compared with those with less number of symptoms. The epidemiological results provide strong circumstantial basis for the diagnosis of chronic toxic encephalopathy in the patient, and also indicates a need for vigilance of the hazards of central nervous system disorders in workers with chronic exposure to solvents in singapore.
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9/66. Acute mercury intoxication with lichenoid drug eruption followed by mercury contact allergy and development of antinuclear antibodies.

    A 31-year-old black man was examined for evaluation of a suspected occupational disease. Three years earlier he had been suffering from acute mercury intoxication during work in a mercury recycling factory. skin symptoms then had been a lichenoid drug eruption, patchy alopecia and stomatitis, which had all disappeared rapidly after systemic glucocorticosteroid treatment. The examination revealed positive patch test reactions to metallic mercury and inorganic mercury compounds, an elevated titre of serum antinuclear antibodies and normal IgE levels. The induction of antinuclear antibodies by mercury has been shown in animal experiments. It can be hypothesized that this patient, who may have had an increased individual susceptibility, became allergic to mercury by the mercury intoxication.
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ranking = 1.2
keywords = intoxication
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10/66. Diffuse white matter lesions in carbon disulfide intoxication: microangiopathy or demyelination.

    Long-term exposure to carbon disulfide (CS(2)) 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 CS(2). The brain magnetic resonance images (MRI) showed diffuse hyperintensity lesions in T(2)-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 CS(2) encephalopathy using brain MRI. In addition, the (99m)Tc-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 CS(2), possibly through microangiopathy. In addition, CS(2) poisoning can be considered as one of the causes of chronic leukoencephalopathy.
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ranking = 0.8
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