Household bleaches based on sodium hypochlorite: review of acute toxicology and poison control center experience.

Bleaches based on solutions of sodium hypochlorite (NaOCl) are widely used in the household to disinfect and clean hard surfaces and to bleach the laundry. A review of both published and unpublished toxicological data is presented. In addition, the results of a survey of human accidents with hypochlorite bleaches by the Poison Control Centers of France, Italy, Belgium, Greece, Turkey, Spain and Portugal for the period 1989-1992 are presented. The data show that acute accidental exposure to household bleach in use or in foreseeable misuse situations results, in the great majority of the cases, in minor, transient adverse effects on health, with no permanent sequelae. Ingestion is the most frequent route of exposure, followed by inhalation of gases evolved by mixing sodium hypochlorite bleach with acid or alkaline products. All evidence presented confirms the normal safety profile of hypochlorite-based bleaches to be similar to that of other 'generally recognized as safe' household products.

Effects of softened and unsoftened fabrics on sensitive skin.

The effects of softened fabrics on the skin were evaluated by a forearm wet and dry test, under conditions simulating real-life skin contact with fabrics. 15 volunteers with sensitive skin according to dermatological assessment and their own recognition entered a double-blind 12 day, 3 sessions per day, forearm wetting and drying test, using cotton fabrics washed with a powder detergent and softened or not with a liquid fabric conditioner. To simulate conditions of skin damage, a dilute solution of sodium lauryl sulfate was applied under patch to the forearm before the start of the study. Skin effects were evaluated by visual grading (redness, dryness and smoothness), by noninvasive skin stripping and measuring of Chroma C* (squamometry), and by instrumental measurements (capacitance, transepidermal water loss, and colorimetry). Both the unsoftened and softened fabrics induced no deleterious effects on control or previously irritated skin. Furthermore, a mild beneficial effect was observed with the softened fabrics, particularly on previously irritated skin. The study findings suggest that softened fabrics may exert a reduced frictional effect on the skin.

Effects of softened and unsoftened fabrics on infant skin.

BACKGROUND: The effects of softened and unsoftened fabrics on the skin of infants of 1-12 months of age were evaluated under real life conditions of skin contact with fabrics. METHODS: During 4 weeks, 24 infants wore cotton fabrics washed with a granular detergent on one side of their lower back, and on the other side, cotton fabrics washed with the same detergent and softened with a liquid fabric softener. Skin effects were evaluated by visual grading for redness, dryness, and smoothness, by skin stripping and measuring of Chroma C* (squamometry), by measurements of elasticity and bioelastic ratio, and by instrumental measurements of skin parameters (pH, capacitance, transepidermal water loss (TEWL), and erythema by colorimetry). RESULTS: No deleterious effects were observed in any infant. A decrease in squamometry (Chroma C*) and an increase in capacitance were detected in skin exposed to softened fabrics relative to unsoftened ones. Values of pH tended to be higher in the sites treated with softened versus unsoftened fabrics (pH 6.06 and 5.87, respectively, at end of study). All other parameters showed no significant differences in the two treatment groups. CONCLUSIONS: Neither softened nor unsoftened fabrics produced any adverse effects on the skin of infants after continuous wearing during 29 days. A slight beneficial effect on the infants' skin was observed with softened relative to unsoftened fabrics. Methods measuring the structure and function of the stratum corneum were more sensitive discriminators of the effects of fabrics on the skin than traditional methods of visual clinical evaluation.

Iron uptake in Plesiomonas shigelloides: cloning of the genes for the heme-iron uptake system.

The iron uptake systems of Plesiomonas shigelloides strains were determined. Siderophore production was not detected by chemical or biological assays, and the strains tested were unable to use enterobactin, aerobactin, or vibriobactin for growth in low-iron media. Both hemin and hemoglobin supported full growth of the bacteria in media lacking other iron sources, but neither transferrin nor lactoferrin served as a source of iron. Hemolysin was detected, and the production of hemolysin was iron repressible. DNA sequences encoding hemolysin production and DNA sequences encoding the ability to use heme or hemoglobin as a sole source of iron were cloned from P. shigelloides and expressed in Escherichia coli. The abilities to use heme and hemoglobin as iron sources were closely linked, and the cloned sequences encoded the ability to transport the porphyrin, as well as iron, into the cells.

A 101-kilodalton heme-binding protein associated with congo red binding and virulence of Shigella flexneri and enteroinvasive Escherichia coli strains.

The ability of Shigella flexneri to bind Congo red or hemin is associated with virulence. A 101-kilodalton (kDa) protein responsible for this phenotype (Crb+) in S. flexneri was identified by a tetramethylbenzidine staining procedure which detects heme-protein complexes in polyacrylamide gels. Labeling of cell-surface polypeptides with 125I revealed that the 101-kDa heme-binding protein is expressed on the cell surface. Expression of the protein was regulated by growth temperature and was found to be encoded by the large virulence plasmid of S. flexneri. Deletion mutants and a Tn5 insertion mutant which were negative for Congo red binding (Crb-) did not express the 101-kDa protein. Enteroinvasive Escherichia coli strains that were Crb+, and whose plasmids shared homology with the S. flexneri virulence plasmid, also expressed the 101-kDa protein. Expression of the protein in S. flexneri and enteroinvasive E. coli correlated with the presence of a 9.2-kilobase EcoRI fragment of these plasmids.

Congo red binding phenotype is associated with hemin binding and increased infectivity of Shigella flexneri in the HeLa cell model.

Wild-type isolates of Shigella flexneri bind the dye Congo red from solid media, thus producing red (Crb+) colonies. Mutants which fail to bind the dye produce white colonies (Crb-) and are avirulent in a variety of systems. In S. flexneri the ability to bind Congo red correlates with the ability to bind hemin and protoporphyrin IX. Binding of hemin by Crb+ S. flexneri was observed both in solid media and in liquid assays. Results of competition experiments suggest that Congo red and hemin bind to the same site on the bacterial cell and are retained on the cell surface. Binding of hemin by Crb+ S. flexneri is independent of hemin transport since both Crb+ and Crb- cells can utilize hemin as a sole source of iron. Both Crb- and Crb- organisms were able to grow in HeLa cell lysates, indicating that the gene(s) that is responsible for Congo red binding does not play a role in the acquisition of intracellular heme iron. By using the HeLa cell invasion system, the effect of hemin prebinding on the invasiveness of Crb+ S. flexneri was determined. Crb+ cells which had prebound hemin exhibited increased invasiveness, indicating a possible role for the crb gene product in the initial stages of invasion by S. flexneri.

Virulence of iron transport mutants of Shigella flexneri and utilization of host iron compounds.

Mutants of Shigella flexneri defective in aerobactin-mediated iron transport were assayed for virulence in several model systems. A Tn5 insertion mutant was invasive in HeLa cells, lethal in the chicken embryo, and produced keratoconjunctivitis in the guinea pig, indicating little or no loss of ability to invade and multiply intracellularly. Although the mutant failed to grow in low-iron medium in vitro, growth equivalent to that of the wild type was observed in HeLa cell lysates. Thus, there appears to be sufficient available iron inside the HeLa cell to allow growth in the absence of siderophore synthesis. Possible host iron sources were tested, and both the mutant and wild type utilized hemin or hematin as a sole source of iron. Only the wild-type, aerobactin-producing strain could remove iron from transferrin or lactoferrin. Two deletion mutants were also assayed for virulence and were found to be avirulent for the chicken embryo. These deletions encompass flanking sequences as well as the aerobactin genes; therefore, adjacent genes may be required for virulence.

Characterization of Shigella flexneri sequences encoding congo red binding (crb): conservation of multiple crb sequences and role of IS1 in loss of the Crb+ phenotype.

The ability to bind Congo red (Crb+) is associated with virulence of Shigella flexneri and is encoded by a large, 220-kilobase plasmid. We cloned fragments of this plasmid to isolate the sequences encoding Congo red binding, to determine the degree of conservation of these sequences among S. flexneri strains, and to study the molecular basis for loss of the Crb+ phenotype. At least two separate BamHI fragments cloned into plasmid vectors encode Congo red binding in E. coli or S. flexneri. One Crb+ clone, pTKS2, contains a copy of IS1 adjacent to the crb sequences. IS1 appears to be responsible for deletions leading to loss of Congo red binding in this clone. In addition, this clone was found to integrate into the chromosome at relatively high frequency. Integration resulted in loss of the Crb+ phenotype. A second clone, pTKS15, which has only limited homology to pTKS2, also encodes Congo red binding. The Crb+ phenotype of transformants carrying pTKS15 was detected at 37 degrees C but not at 30 degrees C, and thus it resembles Congo red binding in wild-type S. flexneri. HindIII digests of plasmid DNA from 10 different S. flexneri strains were hybridized to both of these Crb+ clones and to an IS1 probe. More than one fragment hybridized to pTKS2 or pTKS15. In general, the sizes of these fragments were the same in S. flexneri strains of different serotypes, indicating conservation of these sequences. Three of five copies of IS1 were also found on the large S. flexneri plasmids. Two of the copies were on fragments of the same size in each strain. Analysis of Crb- derivatives of the 10 strains indicated that, although IS1 may be closely linked to crb sequences on the 220-kilobase plasmid, it is not responsible for the majority of deletions of this plasmid associated with loss of Congo red binding.

Cloning the gene for Congo red binding in Shigella flexneri.

The ability to bind the dye Congo red from agar medium is associated with virulence of Shigella species. DNA sequences conferring this property have been cloned from a large, 140-kilobase plasmid of Shigella flexneri into a plasmid vector. This recombinant plasmid does not fully restore virulence to S. flexneri isolates which have lost the large plasmid. This indicates that other genes present on the 140-kilobase plasmid must also be required for virulence of S. flexneri. The cloned fragment contains a copy of the insertion sequence IS1 closely linked to the gene for Congo red binding.