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 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-eight workers from a factory producing nickel-cadmium and other types of batteries came to us for medical evaluation. They included 21 women and 17 men (seniority 2-20 years, age range 31-63 years), and represented a self-selected subset of 700-900 ever-employed and 200+ recently or currently employed workers in the factory. Thirty-four worked on the nickel-cadmium assembly line. Symptoms and signs included: headache in 34; weakness, fatigue and lassitude in 26; dizziness in 16; pruritus and skin eruptions in 37; gingivitis, teeth loss and caries in 34; nasal congestion, nosebleeds and anosmia in 30; cough, phlegm production, wheezing and shortness of breath in 26; "asthma" in 14; bone pain in 18; urinary frequency, beta 2 microglobulinuria and kidney stones in 17; and sterility or multiple abortions (33) in 8 of 21 women. One additional patient had died from an "amyotrophic lateral sclerosis-like syndrome", while CT scans in six workers revealed brain atrophy. One other worker had leukemia, and two had died from cancer (lung and pancreas). Those who had worked for more than 10 years had more symptoms and signs than shorter-term employees, especially neurological illness, bone pain and urinary tract problems, including beta 2 microglobulinuria. Past blood and urinary cadmium levels were in the range of 1.6-8.7 micrograms/dl and 8-306 micrograms/l, respectively. Our findings indicated that: a) health risks for workers were not confined to the nickel-cadmium assembly line or to older workers, b) hazardous exposures still existed and illness appeared in new workers after a clean-up and intervention program, and c) exposures involved increased risks for renal disease and cancers. Finally, there is a need to control exposures and determine health risks in the full cohort of those ever employed, in the workers' children, and in the surrounding environment (air, ground, water) due to the dumping of waste from the plant.
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PMID:Medical findings in nickel-cadmium battery workers. 142 13

Thirty-two workers in an electroplating plant accidently drank water contaminated with nickel sulfate and chloride (1.63 g Ni/liter). Twenty workers promptly developed symptoms (e.g., nausea, vomiting, abdominal discomfort, diarrhea, giddiness, lassitude, headache, cough, shortness of breath) that typically lasted a few hours but persisted 1-2 days in 7 cases. The Ni doses in workers with symptoms were estimated to range from 0.5 to 2.5 g. In 15 exposed workers who were tested on day 1 postexposure, serum Ni concentrations ranged from 13 to 1,340 micrograms/liter and urine Ni concentrations ranged from 0.15 to 12 mg/g creatinine. Ten subjects (with initial urine Ni concentrations greater than 0.8 mg/g creatinine) were hospitalized and treated for 3 days with intravenous fluids to induce diuresis, resulting in a mean elimination half-time (T1/2) for serum Ni of 27 hours (SD +/- 7 hour), which was significantly shorter (p less than .001) than the mean T1/2 of 60 hours (SD +/- 11 hours) in 11 subjects who did not receive intravenous fluids. Laboratory tests showed transiently elevated levels of blood reticulocytes (N = 7), urine albumin (N = 3), and serum bilirubin (N = 2). All subjects recovered rapidly, without evident sequellae, and returned to work by the eighth day after exposure.
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PMID:Acute nickel toxicity in electroplating workers who accidently ingested a solution of nickel sulfate and nickel chloride. 318 43

The effects and clearance of intratracheally instilled nickel subsulfide (Ni3S2) and titanium dioxide (TiO2) were compared. Instilled Ni3S2 was acutely toxic to mice. Blood was recovered from the lungs during lavage, pulmonary polymorphonuclear leukocyte cell levels were increased, body weights decreased, and mice appeared clinically sick. These effects were in contrast to TiO2-instilled animals, which appeared similar to phosphate-buffered saline-instilled controls. The clearance of instilled particles from the lungs was examined for both Ni3S2- and TiO2-exposed mice. Particles were rapidly cleared to the gastrointestinal (GI) tract within 15 min; this clearance was nonspecific for Ni or Ti and appeared to be due to the coughing reflex. Significantly less Ni was present compared with TiO2 in mouse lungs at 3 and 7 days postexposure (P less than 0.05), with halflifes for the later clearance phase of 119 and 462 hr, respectively. Much of the early Ni lung burden was cleared to the GI tract, and Ni levels in the kidney and blood peaked at 1 hr. Longer-term Ni clearance rate constants were similar for lung, kidney, and blood and were consistent with the hypothesis that 63Ni was first solubilized in the lung then transported through the blood.
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PMID:The pulmonary effects and clearance of intratracheally instilled Ni3S2 and TiO2 in mice. 380 46

A 16-year-old male, an industrial high school student working at an ironworks, without a dust mask, began to complain of dry cough and fever several hours after inhalation of stainless steel dusts including 0.1% nickel. A chest X-ray film revealed ground glass shadows, patchy shadows and Kerley B lines in the right lung fields. A high resolution chest CT scan showed fusing panlobular densities, thickening of bronchial walls and thickening of interlobular septa. Blood cells counts revealed leucocytosis with eosinophilia. Arterial blood gas analysis revealed hypoxemia. A bronchoalveolar lavage fluid specimen showed a marked increase in the total cell count and in eosinophils. A transbronchial biopsy specimen showed eosinophilic and lymphocytic infiltration in the alveolar septa. Steroid therapy with methylpredonisolne (250 mg x three days) resulted in clinical remission. As we suspected nickel-induced eosinophilic pneumonia, an inhalation provocation test with 0.5% nickel sulfate solution was carried out with the patient's informed consent. Six hours after inhalation he developed a dry cough and fever with leucocytosis and A-aDo2 widening. The positive results of the inhalation provocation test provided a definite diagnosis of nickel induced eosinophilic pneumonia. A review of the world literature revealed three case reports of nickel induced PIE syndrome, all of whom were clinically diagnosed without biopsy however. We believe that this is the first case diagnosed by transbronchial biopsy-proven tissue eosinophilia and a positive nickel inhalation provocation test.
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PMID:[A case of eosinophilic pneumonia caused by inhalation of nickel dusts]. 808 5

In the last few years, many studies have been carried out concerning the effects of fumes from stainless steel (SS) welding on the health of welders. The respiratory effects of exposure to SS welding fumes have already been studied, but the results of lung function investigations have not been consistent. However, the main factor of risk for the welders' health seems to be related to the great concentration of chromium and nickel contained in fumes coming from SS welding. The aim of this study was to detect the chronic effects of SS welding exposure on pulmonary symptoms and ventilatory function tests. Respiratory symptoms and lung function tests were studied in 134 SS welders and 252 controls (C). Welders and controls were of similar average age, height, and duration in employment. The smoking habits of the groups were also similar. The medical questionnaire on respiratory symptoms was a version of the Medical Research Council questionnaire, modified by the British Occupational Hygiene Society. The flow-volume curves were performed with a calibrated pneumotachograph spirometer before each subject started working. After adjustment for tobacco habits, the SS welders presented a higher prevalence of bronchial irritative symptoms such as cough (P = 0.01) or sputum production (P = 0.02) than the controls. On the other hand, chronic bronchitis appeared to be significantly linked to tobacco consumption. The pulmonary function analysis underscored no significant difference between stainless steel welders and controls (forced expiratory volume in one second, observed/predicted: SS = 0.99 vs C = 0.98; maximal midexpiratory flow, observed/predicted: SS = 0.90 vs C = 0.92; maximal expiratory flow at 50 % of the forced vital capacity, observed/predicted: SS = 0.95 vs C = 0.95). On the other hand, by the mean of the two-ways analysis, a significant tobacco effect was found, without exposure or interaction of tobacco-exposure effects. There was no influence of the specific welding processes on the spirographic parameters, but a decrease in spirographic values after 25 years of welding activity was evident. The results of multiple regression indicated that age was not a confounding factor.
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PMID:Respiratory symptoms and pulmonary function among stainless steel welders. 953 Oct 93

A 44-year-old patient died from amyotrophic lateral sclerosis (ALS) after nine years of heavy exposure to cadmium (Cd) in a nickel cadmium (Ni-Cd) battery factory. Two years after starting work he and co-workers had experienced pruritus, loss of smell, nasal congestion, nosebleeds, cough, shortness of breath, severe headaches, bone pain, and proteinuria. Upper back pain and muscle weakness progressed to flaccid paralysis. EMG findings were consistent with motor neuron disease. Cd impairs the blood-brain barrier, reduces levels of brain copper-zinc (Cu-Zn) superoxide dismutase (SOD), and enhances excitoxicity of glutamate via up-regulation of glutamate dehydrogenase and down-regulation of glutamate uptake in glial cells. High levels of methallothionein, a sign of exposure to heavy metals, have been found in brain tissue of deceased ALS patients. The effects of Cd on enzyme systems that mediate neurotoxicity and motor neuron disease suggest a cause effect relationship between Cd and ALS in this worker.
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PMID:Amyotrophic lateral sclerosis in a battery-factory worker exposed to cadmium. 1137 40

It is a case report on a 55-year-old non-smoking female, dental technician, with a 36-year history of cobalt exposure. The patient suffered from dyspnea, coughing and decrease in physical load tolerance about 20 years after the first occupational contact with cobalt-containing metal dentures. Skin tests performed with a battery of common allergens (metals: nickel, chrome, cobalt; acrylates; disinfectants; and natural rubber latex) were negative. In the patient, interstitial radiological changes, respiratory insufficiency and decrease in diffusion capacity were observed. While performing a provocation test with 0.05% cobaltous chloride, the patient developed dyspnea with concomitant decrease in 1 second forced expiratory volume (FEV1) and peak respiratory flow (PEF) from the beginning of the 3rd hour after provocation and maximum intensity at the 8th hour. These symptoms persisted until the 24th hour. The authors conclude that occupational exposure of the dental technician to cobalt dust derived from metal dentures may cause chronic airway disease with interstitial inflammation, fibrosis and occupational asthma.
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PMID:[Occupational asthma and interstitial cobalt-induced changes in a dental technician: a case report]. 1292 99

Even in the twenty-first century, welding is still a common and a highly skilled occupation. The hazardous agents associated with welding processes are acetylene, carbon monoxide, oxides of nitrogen, ozone, phosgene, tungsten, arsenic, beryllium, cadmium, chromium, cobalt, copper, iron, lead, manganese, nickel, silver, tin, and zinc. All welding processes involve the potential hazards for inhalation exposures that may lead to acute or chronic respiratory diseases. According to literature described earlier it has been suggested that welding fumes cause the lung function impairment, obstructive and restrictive lung disease, cough, dyspnea, rhinitis, asthma, pneumonitis, pneumoconiosis, carcinoma of the lungs. In addition, welding workers suffer from eye irritation, photokeratitis, cataract, skin irritation, erythema, pterygium, non-melanocytic skin cancer, malignant melanoma, reduced sperm count, motility and infertility. Most of the studies have been attempted previously to evaluate the effects of welding fumes. However, no collectively effort illuminating the general effects of welding fumes on different organs or systems or both in human has not been published. Therefore, the aim of this review is to gather the potential toxic effects of welding fumes documented by individual efforts and provide informations to community on hazards of welding.
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PMID:Health hazards of welding fumes. 1464 49

Residents of the Selebi Phikwe area, Botswana where nickel-copper (Ni-Cu) is being exploited often exhibit symptoms of varied degrees of ailments, sicknesses and diseases. A need to investigate their general health status was therefore eminent. Primary data was obtained by means of a questionnaire and structured interviews conducted with individuals, health service providers, business enterprises and educational Institutions. The generated data revealed common ailments, sicknesses and diseases in the area with the four most frequent health complaints being frequent coughing headaches, influenza/common colds and rampant chest pains. Research findings indicated that residents had respiratory tract-related problems, suspected to be linked to the effects of air pollution caused by the emission of sulphur dioxide (SO2) from mining and smelting activities. Residents were frequently in contact with SO2 and related gases and fumes, mineral and silica dust generated from the mining processes. No clearly demarcating differences were noticed in the health status of residents living in the control site from those in the main study area. However, sites most affected were those close to where Ni-Cu is exploited. Environmental factors resulting from mining and smelting activities, among others, could be contributory to the negative health effects occurring at Selebi Phikwe.
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PMID:General health status of residents of the Selebi Phikwe Ni-Cu mine area, Botswana. 1641 54

Two male industrial painters were admitted to hospital with dry cough and dyspnoea on exertion following a tank coating operation using a high-temperature spray paint consisting of a nickel-chromium alloy. Both patients showed hypoxaemia, peripheral leukocytosis, high levels of serum cytokines and bilateral ground-glass opacities on a chest CT scan. They were diagnosed with interstitial pneumonia caused by inhalation of nickel and chrome fumes and successfully treated with corticosteroid. These are rare cases of interstitial pneumonia associated with nickel/chromium inhalation.
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PMID:Interstitial pneumonia caused by inhalation of fumes of nickel and chrome. 1705 14


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