Bromine Exposure Research Articles

Myocardial SERCA2 Protects Against Cardiac Damage and Dysfunction Caused by Inhaled Bromine.

Myocardial sarcoendoplasmic reticulum calcium ATPase 2 (SERCA2) activity is critical for heart function. We have demonstrated that inhaled halogen (chlorine or bromine) gases inactivate SERCA2, impair calcium homeostasis, increase proteolysis, and damage the myocardium ultimately leading to cardiac dysfunction. To further elucidate the mechanistic role of SERCA2 in halogen-induced myocardial damage, we used bromine-exposed cardiac-specific SERCA2 knockout (KO) mice [tamoxifen-administered SERCA2 (flox/flox) Tg (αMHC-MerCreMer) mice] and compared them to the oil-administered controls. We performed echocardiography and hemodynamic analysis to investigate cardiac function 24 hours after bromine (600 ppm for 30 minutes) exposure and measured cardiac injury markers in plasma and proteolytic activity in cardiac tissue and performed electron microscopy of the left ventricle (LV). Cardiac-specific SERCA2 knockout mice demonstrated enhanced toxicity to bromine. Bromine exposure increased ultrastructural damage, perturbed LV shape geometry, and demonstrated acutely increased phosphorylation of phospholamban in the KO mice. Bromine-exposed KO mice revealed significantly enhanced mean arterial pressure and sphericity index and decreased LV end diastolic diameter and LV end systolic pressure when compared with the bromine-exposed control FF mice. Strain analysis showed loss of synchronicity, evidenced by an irregular endocardial shape in systole and irregular vector orientation of contractile motion across different segments of the LV in KO mice, both at baseline and after bromine exposure. These studies underscore the critical role of myocardial SERCA2 in preserving cardiac ultrastructure and function during toxic halogen gas exposures. SIGNIFICANCE STATEMENT: Due to their increased industrial production and transportation, halogens such as chlorine and bromine pose an enhanced risk of exposure to the public. Our studies have demonstrated that inhalation of these halogens leads to the inactivation of cardiopulmonary SERCA2 and results in calcium overload. Using cardiac-specific SERCA2 KO mice, these studies further validated the role of SERCA2 in bromine-induced myocardial injury. These studies highlight the increased susceptibility of individuals with pathological loss of cardiac SERCA2 to the effects of bromine.

Sex differences in cardiopulmonary effects of acute bromine exposure.

Accidental occupational bromine (Br>2>) exposures are common, leading to significant morbidity and mortality; however, the specific effects of Br>2> inhalation in female victims are unclear. Our studies demonstrated that acute high-concentration Br>2> inhalation is fatal, and cardiac injury and dysfunction play an important role in Br>2> toxicity in males. In this study, we exposed female Sprague Dawley rats, age-matched to those males from previously studied, to 600ppm Br>2> for 45min and assessed their survival, cardiopulmonary injury and cardiac function after exposure. Br>2> exposure caused serious mortality in female rats (59%) 48h after exposure. Rats had severe clinical distress, reduced heart rates and oxygen saturation after Br>2> inhalation as was previously reported with male animals. There was significant lung injury and edema when measured 24h after exposure. Cardiac injury biomarkers were also significantly elevated 24h after Br>2> inhalation. Echocardiography and hemodynamic studies were also performed and revealed that the mean arterial pressure was not significantly elevated in females. Other functional cardiac parameters were also altered. Aside from the lack of elevation of blood pressure, all other changes observed in female animals were also present in male animals as reported in our previous study. These studies are important to understand the toxicity mechanisms to generate therapies and better-equip first responders to deal with these specific scenarios after bromine spill disasters.>.

Behavioral and Neuronal Effects of Inhaled Bromine Gas: Oxidative Brain Stem Damage.

The risk of accidental bromine (Br2) exposure to the public has increased due to its enhanced industrial use. Inhaled Br2 damages the lungs and the heart; however, adverse effects on the brain are unknown. In this study, we examined the neurological effects of inhaled Br2 in Sprague Dawley rats. Rats were exposed to Br2 (600 ppm for 45 min) and transferred to room air and cage behavior, and levels of glial fibrillary acidic protein (GFAP) in plasma were examined at various time intervals. Bromine exposure resulted in abnormal cage behavior such as head hitting, biting and aggression, hypervigilance, and hyperactivity. An increase in plasma GFAP and brain 4-hydroxynonenal (4-HNE) content also was observed in the exposed animals. Acute and delayed sympathetic nervous system activation was also evaluated by assessing the expression of catecholamine biosynthesizing enzymes, tryptophan hydroxylase (TrpH1 and TrpH2), and tyrosine hydroxylase (TyrH), along with an assessment of catecholamines and their metabolites. TyrH was found to be increased in a time-dependent manner. TrpH1 and TrpH2 were significantly decreased upon Br2 exposure in the brainstem. The neurotransmitter content evaluation indicated an increase in 5-HT and dopamine at early timepoints after exposure; however, other metabolites were not significantly altered. Taken together, our results predict brain damage and autonomic dysfunction upon Br2 exposure.

Degradation of Polyamide Nanofiltration Membranes by Bromine: Changes of Physiochemical Properties and Filtration Performance.

The potential coexistence and interaction of bromine and polyamide membranes during membrane-based water treatment prompts us to investigate the effect of bromine on membrane performance. For fully aromatic polyamide membrane NF90 exposed under a mild bromination condition (10 mg/L), bromine incorporation resulted in more negatively charged (-13 vs -25 mV) and hydrophobic (55.2 vs 58.9°) surfaces and narrower pore channels (0.3 vs 0.29 nm). The permeabilities of water and neutral solutes were reduced by 64 and 69-87%, respectively, which was attributed to the decreased effective pore radius and hydrophilicity. NaCl permeability was reduced by 90% as a synergistic result of enhanced size exclusion and charge repulsion. The further exposure (100 and 500 mg/L bromine) resulted in a more hydrophobic surface (61.7 and 65.5°) and the minor further reduction for water and solute permeabilities (1-9%). Compared with chlorine, the different incorporation efficiency and properties (e.g., atomic size, hydrophilicity) of bromine resulted in opposite trends and/or different degrees for the variation of physicochemical properties and filtration performance of membranes. The bromine incorporation, the shift and disappearance of three characteristic bands, and the increased O/N ratio and calcium content indicated the degradation pathways of N-bromination and bromination-promoted hydrolysis under mild bromination conditions (480 mg/L·h). The further ring-bromination occurred after severe bromine exposure (4800-24,000 mg/L·h). The semi-aromatic polyamide membrane NF270 underwent a similar but less significant deteriorated filtration performance compared with NF90, which requires a different explanation.

Chronic cardiac structural damage, diastolic and systolic dysfunction following acute myocardial injury due to bromine exposure in rats.

Accidental bromine spills are common and its large industrial stores risk potential terrorist attacks. The mechanisms of bromine toxicity and effective therapeutic strategies are unknown. Our studies demonstrate that inhaled bromine causes deleterious cardiac manifestations. In this manuscript we describe mechanisms of delayed cardiac effects in the survivors of a single bromine exposure. Rats were exposed to bromine (600ppm for 45min) and the survivors were sacrificed at 14 or 28days. Echocardiography, hemodynamic analysis, histology, transmission electron microscopy (TEM) and biochemical analysis of cardiac tissue were performed to assess functional, structural and molecular effects. Increases in right ventricular (RV) and left ventricular (LV) end-diastolic pressure and LV end-diastolic wall stress with increased LV fibrosis were observed. TEM images demonstrated myofibrillar loss, cytoskeletal breakdown and mitochondrial damage at both time points. Increases in cardiac troponin I (cTnI) and N-terminal pro brain natriuretic peptide (NT-proBNP) reflected myofibrillar damage and increased LV wall stress. LV shortening decreased as a function of increasing LV end-systolic wall stress and was accompanied by increased sarcoendoplasmic reticulum calcium ATPase (SERCA) inactivation and a striking dephosphorylation of phospholamban. NADPH oxidase 2 and protein phosphatase 1 were also increased. Increased circulating eosinophils and myocardial 4-hydroxynonenal content suggested increased oxidative stress as a key contributing factor to these effects. Thus, a continuous oxidative stress-induced chronic myocardial damage along with phospholamban dephosphorylation are critical for bromine-induced chronic cardiac dysfunction. These findings in our preclinical model will educate clinicians and public health personnel and provide important endpoints to evaluate therapies.

Vascular permeability disruption explored in the proteomes of mouse lungs and human microvascular cells following acute bromine exposure.

Bromine (Br2) is an organohalide found in nature and is integral to many manufacturing processes. Br2 is toxic to living organisms, and high concentrations can prove fatal. To meet industrial demand, large amounts of purified Br2 are produced, transported, and stored worldwide, providing a multitude of interfaces for potential human exposure through either accidents or terrorism. To identify the key mechanisms associated with acute Br2 exposure, we have surveyed the lung proteomes of C57BL/6 male mice and human lung-derived microvascular endothelial cells (HMECs) at 24 h following exposure to Br2 in concentrations likely to be encountered in the vicinity of industrial accidents. Global discovery proteomics applications combined with systems biology analysis identified robust and highly significant changes in proteins associated with three biological processes: 1) exosome secretion, 2) inflammation, and 3) vascular permeability. We focused on the latter, conducting physiological studies on isolated perfused lungs harvested from mice 24 h after Br2 exposure. These experiments revealed significant increases in the filtration coefficient (Kf) indicating increased permeability of the pulmonary vasculature. Similarly, confluent monolayers of Br2 and Br-lipid-treated HMECs exhibited differential levels of zona occludens-1 that were found to be dissociated from cell wall localization, an increase in phosphorylation and internalization of E-cadherin, as well as increased actin stress fiber formation, all of which are consistent with increased permeability. Taken as a whole, our discovery proteomics and systems analysis workflow, combined with physiological measurements of permeability, revealed both profound and novel biological changes that contribute to our current understanding of Br2 toxicity.

Bromine Exposure In Pregnant Mice May Reduce VEGF Signaling Via Increased Circulating VEGF Decoy Receptor sFlt‐1

Inhalation of oxidant gas and vapor like the halogen bromine (Br2) may pose an increased threat to pregnant women and their unborn fetuses. We recently published that pregnant (P) C57Bl/6 mice exposed to 600 ppm Br2 for 30 minutes on gestational day 14.5 (E14.5) exhibited increased mortality, lung injury, and blood pressure at E18.5 when compared to similarly exposed non‐pregnant (NP) mice. Additionally, fetuses of Br2‐exposed pregnant mice displayed severe growth restriction, which cumulatively indicated a preeclampsia‐like phenotype. Administration of the phosphodiesterase 5 (PDE5) inhibitor tadalafil abrogated or significantly mitigated these effects in Br2‐exposed pregnant mice but had no effect on non‐pregnant counterparts. We hypothesize that exposure to Br2 via inhalation in pregnant mice results in placental damage and subsequent release of anti‐angiogenic molecules into maternal circulation resulting in systemic endothelial dysfunction and a vasoconstrictive environment mediated by dysfunctional VEGF signaling. Firstly, we have identified significant increases at 0.5 h post‐Br2 exposure of circulating brominated fatty acids and fatty acid aldehydes (2‐BrPA and 2‐BrPALD) as well as their glutathionylated species at 6h. These may serve as potential biomarkers and/or mediators of Br2‐inhalation induced systemic injury. Furthermore, preliminary results indicate aortas incubated ex vivo in the presence of 2‐BrPA and 2‐BrPALD are more sensitive to the vasoconstricting agent phenylephrine and less sensitive to the vasodilator acetylcholine. Similarly, aortas pregnant mice exposed to Br2 are less sensitive to acetylcholine when compared with similarly exposed non‐pregnant mice. Secondly, utilizing time‐course measurements, we have identified increases in the circulating VEGF decoy receptor sFlt‐1 beginning at 72h post‐exposure in pregnant mice. No increase is observed in similarly exposed non‐pregnant mice (PBr272h 7280.3 ± 1592 vs NPBr272h 1233.5 ± 1063 pg/mL p≤0.001). Additionally, this time point also coincides with a pregnancy specific increase in lung edema/injury as evidenced by lung wet:dry weight ratios (P Br272h 4.68 ± 0.10 vs NP Br272h 4.22 ± 0.04 p≤0.05). Lastly, supplementation of exogenous VEGF‐121 intended to overcome the effects of increased circulating sFlt‐1 improves both survival and weight gain profiles of pregnant mice exposed to Br2 as well as their fetuses. This study implicates diminished VEGF signaling in pregnancy specific Br2 inhalation injury contributing to increased blood pressures, lung injury and subsequent mortality.Support or Funding InformationNIEHS CounterACT ‐5U01ES026458 02, 1 U01 ES027697 01, Ruth L. Kirschstein National Research Service Award Institutional Training Grant ‐ T32HL007918.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Bromofatty aldehyde derived from bromine exposure and myeloperoxidase and eosinophil peroxidase modify GSH and protein

α-Chlorofatty aldehydes (α-ClFALDs) and α-bromofatty aldehydes (α-BrFALDs) are produced in activated neutrophils and eosinophils. This study investigated the ability of α-BrFALD and α-ClFALD to react with the thiols of GSH and protein cysteinyl residues. Initial studies showed that 2-bromohexadecanal (2-BrHDA) and 2-chlorohexadecanal (2-ClHDA) react with GSH producing the same fatty aldehyde-GSH adduct (FALD-GSH). In both synthetic and cellular reactions, FALD-GSH production was more robust with 2-BrHDA compared with 2-ClHDA as precursor. NaBr-supplemented phorbol myristate acetate (PMA)-activated neutrophils formed more α-BrFALD and FALD-GSH compared with non-NaBr-supplemented neutrophils. Primary human eosinophils, which preferentially produce hypobromous acid and α-BrFALD, accumulated FALD-GSH following PMA stimulation. Mice exposed to Br2 gas had increased levels of both α-BrFALD and FALD-GSH in the lungs, as well as elevated systemic plasma levels of FALD-GSH in comparison to mice exposed to air. Similar relative reactivity of α-ClFALD and α-BrFALD with protein thiols was shown using click analogs of these aldehydes. Collectively, these data demonstrate that GSH and protein adduct formation are much greater as a result of nucleophilic attack of cysteinyl residues on α-BrFALD compared with α-ClFALD, which was observed in both primary leukocytes and in mice exposed to bromine gas.

Comparison of interaction mechanisms of copper phthalocyanine and nickel phthalocyanine thin films with chemical vapours

The present study deals with comparing interaction mechanisms of copper phthalocyanine and nickel phthalocyanine with versatile chemical vapours: reducing, stable aromatic and oxidizing vapours namely; diethylamine, benzene and bromine. The variation in electrical current of phthalocyanines with exposure of chemical vapours is used as the detection parameter for studying interaction behaviour. Nickel phthalocyanine is found to exhibit anomalous behaviour after exposure of reducing vapour diethylamine due to alteration in its spectroscopic transitions and magnetic states. The observed sensitivities of copper phthalocyanine and nickel phthalcyanine films are different in spite of their similar bond numbers, indicating significant role of central metal atom in interaction mechanism. The variations in electronic transition levels after vapours exposure, studied using UV–Visible spectroscopy confirmed our electrical sensing results. Bromine exposure leads to significant changes in vibrational bands of metal phthalocyanines as compared to other vapours.

161 - Bromine Exposure in Pregnant Mice May Reduce VEGF Signaling Via Increased Circulating VEGF Decoy Receptor sFLT-1

Inhalation of oxidant gas and vapor like the halogen bromine (Br2) may pose an increased threat to pregnant women and their unborn fetuses. We recently published that pregnant (P) C57Bl/6 mice exposed to 600ppm Br2 for 30 minutes on gestational day 14.5 (E14.5) exhibited increased mortality, lung injury, and blood pressure at E18.5 when compared to similarly exposed non-pregnant (NP) mice. Additionally, fetuses of Br2-exposed pregnant mice displayed severe growth restriction, which cumulatively indicated a preeclampsia-like phenotype. Administration of the phosphodiesterase 5 (PDE5) inhibitor tadalafil abrogated or significantly mitigated these effects in Br2-exposed pregnant mice but had no effect on non-pregnant counterparts. We hypothesize that exposure to Br2 via inhalation in pregnant mice results in placental damage and subsequent release of anti-angiogenic molecules into maternal circulation resulting in systemic endothelial dysfunction and a vasoconstrictive environment mediated by dysfunctional VEGF signaling. Firstly, we have identified significant increases at 0.5h post-Br2 exposure of circulating brominated fatty acids and fatty acid aldehydes (2-BrPA and 2-BrPALD) as well as their glutathionylated species at 6h. These may serve as potential biomarkers and/or mediators of Br2-inhalation induced systemic injury. Furthermore, preliminary results indicate aortas incubated ex vivo in the presence of 2-BrPA and 2-BrPALD are more sensitive to the vasoconstricting agent phenylephrine and less sensitive to the vasodilator acetylcholine. Secondly, utilizing time-course measurements, we have identified increases in the circulating VEGF decoy receptor sFLT-1 beginning at 72h post-exposure in pregnant mice. No increase is observed in similarly exposed non-pregnant mice (PBr272h 7280.3 ± 1592 vs NPBr272h 1233.5 ± 1063 pg/mL p≤0.001). Additionally, this time point also coincides with a pregnancy specific increase in lung edema/injury as evidenced by lung wet:dry weight ratios (P Br272h 4.68 ± 0.10 vs NP Br272h 4.22 ± 0.04 p≤0.05). This study implicates diminished VEGF signaling in pregnancy specific Br2 inhalation injury contributing to increased blood pressures, lung injury and subsequent mortality.

A dynamic system for delivering controlled bromine and chlorine vapor exposures to weanling swine skin

Context: Assessing the hazards of accidental exposure to toxic industrial chemical (TIC) vapors and evaluating therapeutic compounds or treatment regimens require the development of appropriate animal models.Objective: The objective of this project was to develop an exposure system for delivering controlled vapor concentrations of TICs to the skin of anesthetized weanling pigs. Injury levels targeted for study were superficial dermal (SD) and deep dermal (DD) skin lesions as defined histopathologically.Materials and methods: The exposure system was capable of simultaneously delivering chlorine or bromine vapor to four, 3-cm diameter exposure cups placed over skin between the axillary and inguinal areas of the ventral abdomen. Vapor concentrations were generated by mixing saturated bromine or chlorine vapor with either dried dilution air or nitrogen.Results: Bromine exposure concentrations ranged from 6.5 × 10−4 to 1.03 g/L, and exposure durations ranged from 1 to 45 min. A 7-min skin exposure to bromine vapors at 0.59 g/L was sufficient to produce SD injuries, while a 17-min exposure produced a DD injury. Chlorine exposure concentrations ranged from 1.0 to 2.9 g/L (saturated vapor concentration) for exposures ranging from 3 to 90 min. Saturated chlorine vapor challenges for up to 30 min did not induce significant dermal injuries, whereas saturated chlorine vapor with wetted material on the skin surface for 30–60 min induced SD injuries. DD chlorine injuries could not be induced with this system.Conclusion: The vapor exposure system described in this study provides a means for safely regulating, quantifying and delivering TIC vapors to the skin of weanling swine as a model to evaluate therapeutic treatments.

Gene expression analysis of bromine-induced burns in porcine skin

Bromine is an industrial chemical that is irritating to the skin and causes cutaneous burns. An important factor in selecting or developing an effective treatment is to understand the underlying molecular mechanisms of tissue damage and wound healing. This study used a weanling swine burn model and microarray analysis to evaluate the effect of exposure length and sampling times on the transcriptional changes in response to cutaneous bromine injury. Ventral abdominal sites ( N = 4/treatment group) were exposed to 600 μL undiluted bromine for 45 s or 8 min. At 24 h and 7 d post-exposure, total RNA from skin samples was isolated, processed, and hybridized to Affymetrix GeneChip ® Porcine Genome Arrays. Expression analysis revealed that bromine exposure duration appeared to have less effect on the transcript changes than the sampling time. The percent transcripts changed at 24 h were similar (30%) whether having a 45 s or 8 min bromine exposure; percent transcripts changed at 7 d were also similar (62%) regardless of exposure length. However, only 13–14% of the transcripts were similar when comparing samples analyzed at 24 h and 7 d. Ingenuity Pathways Analysis (IPA) revealed six common biological functions among the top 10 functions of each experimental group, while canonical pathway analysis revealed 11 genes that were commonly shared among 24 significantly altered signaling pathways. Additionally, there were 11 signaling pathways in which there were no commonly shared transcripts. The present study is an initial assessment of the transcriptional responses to cutaneous bromine exposure identifying molecular networks and genes that could serve as targets for developing therapeutics for bromine-induced skin injury.

Effect of long-term administration of arsenic (III) and bromine with and without selenium and iodine supplementation on the element level in the thyroid of rat

The aim of this study was to evaluate the influence of arsenic and bromine exposure with or without iodine and selenium supplementation on the element level in the thyroid of rats. Four major groups of Wistar female rats were fed with respective diets: group A - standard diet, group B - iodine rich diet (10 mg I/kg food), group C - selenium rich diet (1 mg Se/kg) and group D - iodine and selenium rich diet (as in group B and C). Each group was divided into four subgroups per 7 animals each receiving either NaAsO(2) ip (6.5 mg.kg(-1) twice a week for two weeks and 3.25 mg.kg(-1) for six weeks) or KBr in drinking water (58.8 mg.l(-1)) for 8 weeks or combined administration of both substances. Remaining subgroup served as controls. After 8 weeks thyroid glands were analyzed by ICP-MS for As, Br, Se, and I content. The exposition of rat to arsenic or bromine causes the accumulation of these elements in the thyroid gland ( approximately 18 ppm of As, approximately 90 ppm of Br) and significantly affects iodine and selenium concentration in the thyroid. In iodine and/or selenium supplemented rats the bromine intake into the thyroid was lowered to approximately 50% of the level in unsupplemented animals. Also selenium thyroid level elevated due to KBr administration was lowered by iodine supplementation in the diet. The accumulation of arsenic in the thyroid was not influenced by selenium or iodine supplementation; however, As(III) administration increased iodine thyroid level and suppressed selenium thyroid level in selenium or iodine supplemented group of animals.

Accidental bromine exposure in an urban population: an acute epidemiological assessment.

In November 1984, because of an accident at a chemical plant, the population of a large area in the town of Geneva, Switzerland, was exposed to toxic bromine gas during several hours at concentrations above the short-term exposure limit. We describe the development of the disaster, the reactions of the fire brigade, the police and the first aid services as well as the breakdown of communications that occurred. On-the-spot epidemiological assessment of the exposed area and of the characteristics of the exposure syndrome was combined with the emergency care of 91 self-referred patients that were seen at the University Hospital. Follow-up was obtained one month later. The clinical course was moderate (eyes and upper airways irritation) and self-limiting in all cases. Immediate definition of the exposed population permitted effective follow-up. Such early evaluation could prove to be of crucial importance for managing more serious accidents of a similar nature.

Bromine in human tissue

The normal levels of bromine in human tissue are given and their use in the interpretation of levels found when over-exposure is a possibility is described. Bromine is "normally" distributed in human tissue as are essential trace elements. This allows a bromine (microgram) to chlorine (mg) ratio to be established (3.2) above which bromine exposure must be considered. The bromine concentrations in sections of hair can be used to establish the time of administration even when small amounts are ingested, but owing to the long half-life (about 15 days) found in human tissue interpretation after multiple doses may be difficult.

Intercalation of bromine into natural graphite the effect of oxidation and residual bromine on the rate and amount of uptake

Intercalation of bromine at 20°C into spectroscopic grade SP-1 natural graphite flakes oxidized previously to four levels of burn-off has been studied. The threshold pressure, equilibrium amounts taken up at relative pressures up to 0.95, and the diffusion coefficient for bromine uptake are little affected by graphite oxidation at all burn-off s studied (up to 46.1%). However the time after bromine exposure at the threshold pressure at which rapid bromine intercalation commences monotonically decreases with increasing burn-off. It is suggested that during this initial time period, bromine entering the graphite is essentially fully ionized, whereas bromine entering later, and rapidly, is not ionized. Oxidation affects the subsequent thermal stability of the intercalated bromine and the composition of the residue compound formed following heating to 950°C. Rates of uptake and amount of bromine intercalated subsequently on the residue compounds are dependent upon their Br C ratio and how the residual compounds were formed.

Bromine in human tissue

The normal levels of bromine in human tissue are given and their use in the interpretation of levels found when over-exposure is a possibility is described. Bromine is “normally” distributed in human tissue as are essential trace elements. This allows a bromine (μg) to chlorine (mg) ratio to be established (3.2) above which bromine exposure must be considered. The bromine concentrations in sections of hair can be used to establish the time of administration even when small amounts are ingested, but owing to the long halflife (about 15 days) found in human tissue interpretation after multiple doses may be difficult.

The surface structure of titanium and its interaction with bromine and chlorine

The surface structure and composition of titanium have been studied by electron diffraction and Auger electron spectroscopy in the temperature range 25 to 850°C. Atomically clean, well-defined Ti surfaces were obtained by a combination of argon ion sputtering and thermal treatment at 700 to 800°C. A series of surface superstructures was observed as the crystal temperature was gradually decreased. The development of the superstructures is best explained as due to surface reconstruction as a result of surface relaxation. The interaction of bromine and chlorine vapors with clean Ti surfaces was investigated in the temperature range 25 to 500°C. Bromine exposure at room temperature gave rise to an amorphous surface layer, which on annealing transformed into an epitaxial TiBr 2 structure. Chlorine interaction resulted in the formation of an epitaxial TiCl 3 on both cold and hot Ti surfaces. Surface impurities inhibited the chemical interaction process on the Ti surface.

Nature of the surviving plaque-forming unit of reovirus in water containing bromine.

The initial inactivation of reovirus in water containing 3 to 7 microns M bromine as HOBr was very rapid. Electron microscopy revealed extensive physical damage to the virions in as little as 1 min, but none were degraded beyond recognition. As treatment time continued, the reaction rate decreased toward a plateau of resistance, usually at about the 10-4 survival level; still no particles were lost. Progeny grown from these resistant plaque-forming units (PFU) were no more resistant to HOBr than the parent cultures. Small-number aggregation (adhering groups of two to ten virions counted by electron microscopy) had no detectable effect on the level of persistant PFU. Large aggregates seemed to be involved. Sonic treatment at 20 kHz after bromine exposure increased survival PFU titer 10- to 43-fold. Virus exposed to light centrifugation prior to bromine treatment did not show the plateau of resistance. Surviving PFU sedimented faster in a shallow sucrose gradient than single virions. Large aggregates were apparently too few to be counted by electron microscopy, but their penetration and inactivation must be achieved by any disinfectant chosen to rid water of reovirus.

Nature of the Surviving Plaque-Forming Unit of Reovirus in Water Containing Bromine1

The initial inactivation of reovirus in water containing 3 to 7 microns M bromine as HOBr was very rapid. Electron microscopy revealed extensive physical damage to the virions in as little as 1 min, but none were degraded beyond recognition. As treatment time continued, the reaction rate decreased toward a plateau of resistance, usually at about the 10-4 survival level; still no particles were lost. Progeny grown from these resistant plaque-forming units (PFU) were no more resistant to HOBr than the parent cultures. Small-number aggregation (adhering groups of two to ten virions counted by electron microscopy) had no detectable effect on the level of persistant PFU. Large aggregates seemed to be involved. Sonic treatment at 20 kHz after bromine exposure increased survival PFU titer 10- to 43-fold. Virus exposed to light centrifugation prior to bromine treatment did not show the plateau of resistance. Surviving PFU sedimented faster in a shallow sucrose gradient than single virions. Large aggregates were apparently too few to be counted by electron microscopy, but their penetration and inactivation must be achieved by any disinfectant chosen to rid water of reovirus.