Public health implications of components of plastics manufacture. Flame retardants.
(57/611)
The four processes involved in the flammability of materials are described and related to the various flame retardance mechanisms that may operate. Following this the four practical approaches used in improving flame retardance of materials are described. Each approach is illustrated with a number of typical examples of flame retardants or synthetic procedures used. This overview of flammability, flame retardance, and flame retardants used is followed by a more detailed examination of most of the plastics manufactured in the United States during 1973, their consumption patterns, and the primary types of flame retardants used in the flame retardance of the most used plastics. The main types of flame retardants are illustrated with a number of typical commercial examples. Statistical data on flame retardant market size, flame retardant growth in plastics, and price ranges of common flame retardants are presented. (+info)
Cancer mortality in U.S. counties with plastics and related industries.
(58/611)
Counties in the United States have been identified with chemical establishments whose primary manufacturing processes use vinyl chloride. Site-specific cancer mortality comparisons have revealed an excess of multiple myeloma in males associated with two of the manufacturing categories, synthetic rubber and synthetic fibers. A causal relationship between these manufacturing categories and multiple myeloma could not be established. An industry-based assessment of the occupational contribution to this excess is needed to evaluate the etiologic importance of this relationship. (+info)
Respiratory disease caused by synthetic fibres: a new occupational disease.
(59/611)
Seven patients exposed to the inhalation of synthetic fibres presented with various bronchopulmonary diseases, such as asthma, extrinsic allergic alveolitis, chronic bronchitis with bronchiectasis, spontaneous pneumothorax, and chronic pneumonia. The histological features are described and an attempt has been made to set up immunological techniques for the diagnosis. A series of histochemical techniques, based on textile chemistry, are proposed for the identification of the inclusions found in bronchopulmonary lesions. The results of the experimental production of the disease in guinea-pigs by the inhalation of synthetic fibre dusts are presented. The prognosis of these cases is good in the acute or recently established cases but is poor when widespread and irreversible fibrosis has set in. The authors consider that pulmonary disease due to inhaled particles is probably set off by an individual factor, possibly immunological. (+info)
Cytokines regulate microglial adhesion to laminin and astrocyte extracellular matrix via protein kinase C-dependent activation of the alpha6beta1 integrin.
(60/611)
Microglia are highly plastic cells that participate in inflammatory and injury responses within the CNS and that can migrate extensively after activation. Because astrocytes and their extracellular matrix (ECM) form a large part of the CNS parenchyma, we undertook to study the adhesive interactions between microglia and these substrates in vitro. In contrast to oligodendrocyte precursor cells, microglia formed only weak interactions with astrocytes and their ECM. On specific ECM substrates the microglia adhered strongly to fibronectin, vitronectin, and plastic but only weakly to laminin. Microglial adhesion to laminin was increased significantly by the proinflammatory cytokines TNF, IFN-alpha, and IFN-gamma but was decreased by TGF-beta1, with the TGF-beta1 effect being dominant over the other cytokines. Fluorescence-activated cell sorting (FACS) analysis and immunoprecipitation showed that microglia constitutively express the alpha6beta1 integrin, a well characterized laminin receptor, and that alpha6beta1 expression levels did not change after cytokine treatment. Function-blocking studies showed that microglial adhesion to laminin is mediated entirely by the alpha6beta1 integrin, strongly suggesting that the cytokine regulation of adhesion to laminin is mediated by changes in the activation state of alpha6beta1. Analysis of signaling pathways revealed that activation of alpha6beta1 is mediated by a PKC-dependent mechanism. In light of the evidence that laminin expression is upregulated after CNS injury, the findings suggest that cytokine regulation of microglial adhesion to laminin may play a fundamental role in determining the extent of microglial infiltration into and retention at the site of injury. (+info)
Metal sensitivity in patients with joint replacement arthroplasties.
(61/611)
A high incidence of unexpected metal sensitivity was found in patients with metal-to-metal (McKee) hip arthroplasties. Patients with metal-to-plastic (Charnley) prostheses had no greater incidence of metal sensitivity than a control group awaiting operation. If metal sensitivity does occur loosening of the prosthesis may be a complication. (+info)
Incidence of metal sensitivity in patients with total joint replacements.
(62/611)
Sensitivity to chromium, cobalt, nickel, molybdenum, vanadium, and titanium was studied by patch tests in 50 patients who had received total joint replacements. Nineteen (38%) were sensitive to one or more of the metals. In 23 patients non-traumatic failure of the prosthesis had occurred, and 15 of these patients were sensitive to metal. Out of 27 patients with no evidence of prosthesis loosening, four were sensitive to nickel and cobalt or nickel only. Dermatological reactions occurred in 13 patients after surgery; in only eight, however, was there evidence of metal sensitivity. These findings indicate that metal-on-metal total joint replacements may sensitise the patient to metals contained in the prosthesis. Although there is a high incidence of prosthesis failure among metal-sensitive patients it remains uncertain whether the loosening causes the sensitisation or vice versa. (+info)
Skin problems among fiber-glass reinforced plastics factory workers in Japan.
(63/611)
Two surveys, one in winter the other in summer time, examined the skin problems of the entire manual workers (N=148) from 11 small-to-medium sized fiber-glass reinforced plastics (FRP) factories located in Kyushu, Japan. The workers were exposed to unsaturated polyester resin, including styrene and auxiliary agents such as cobalt naphthenate, hardeners such as methyl ethyl ketone peroxides, glass fiber and dust including shortened glass fiber and plastic particles. Eighty-seven workers (58.8%) reported having skin problems (mainly itching or dermatitis) since they started to work in FRP manufacturing and 25 workers had consulted a physician because of their skin problems; one worker was forced to take sick leave because of his severe dermatitis. History of allergic diseases and shorter occupational period (duration of employment) in a FRP factory were associated with greater probability of having a history of work-related skin symptoms. Workers in factories where dust-generating and lamination sites were located in different buildings were significantly less likely to have a history of skin problems than those in factories where the two sites were located in the same building. Of the 67 workers examined in both seasons closed to double the prevalence of dermatitis was found in summer (23.3%) than winter (13.4%). (+info)
Nickel deficiency and nickel-rhodium interaction in chicks.
(64/611)
Nickel deficiency was produced in chicks under near optimal growth conditions. This judgment is based on the finding that chicks fed the experimental diet supplemented with nickel had a very satisfactory growth rate, over 600 g in 4 weeks. To induce nickel deficiency, chicks were raised in plastic cages located inside plastic isolators and were fed diets (containing 2-15 ng of nickel/g) based on dried skim milk, acid-washed ground corn, EDTA-extracted soy protein, and corn oil. In 2 experiments, controls were fed 3 mug of nickel/g as NiCl2-6H2O. In experiment 3, instead of 1 control group 25, 50, 250, and 2,500 ng/g of supplemental dietary nickel as NiCl2-6H2O were each given to separate groups of chicks. Nickel deprivation resulted in: ultrastructural changes in the liver with the most obvious abnormality in the organization of the rough endoplasmic reticulum; altered gross appearance, reduced oxidative ability, and decreased lipid phosphorus in the liver; altered shank skin pigmentation that was associated with a decrease in yellow lipochrome pigments; and lower hematocrits. Deficiency also tended to increase the thickness of the legs and size of the hock; decrease the length:width ratios of the tibias and femurs; and decrease the plasma cholesterol. None of the signs of deficiency were seen in chicks fed diets containing at least 52 ng of nickel/g. In one experiment, a group of birds was fed 50 mug of rhodium/g of diet as (ClRh(NH3)5)SO4 to ascertain whether rhodium is a metabolic antagonist of nickel. Supplemental rhodium increased the hematocrits and liver oxidative ability of both nickel-deficient and -supplemented chicks, and increased total liver lipids, liver lipid phosphorus, and liver cholesterol in the nickel-deficient chicks alone. Rhodium did not increase the signs of nickel deficiency. (+info)