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Bromide

The bromide ion (Br⁻) is a monovalent halide anion consisting of a single bromine atom with a negative charge, acting as the conjugate base of hydrobromic acid and occurring predominantly in bromide salts.^[1] Bromine, from which bromide derives, is a volatile halogen element with atomic number 35, and bromide ions are highly soluble in water, forming colorless crystals in compounds like sodium bromide and potassium bromide.^[1] Naturally, bromide is abundant in aquatic environments, with concentrations in seawater typically ranging from 66 to 68 mg/L, representing a significant portion of dissolved halides and originating from ancient oceanic deposits and geological processes.^[2] Bromide compounds exhibit versatile chemical reactivity, participating in oxidation-reduction reactions and serving as precursors in organic synthesis due to the ion's nucleophilic properties.^[3] Historically, potassium bromide was extensively used as a sedative and anticonvulsant from the mid-19th century onward, leveraging its central nervous system depressant effects, though chronic administration often resulted in bromism—a toxic syndrome characterized by neurological and dermatological symptoms—leading to its replacement by safer alternatives in human medicine.^[4]^[5] In photography, silver bromide's photosensitivity enabled its role in gelatin emulsions for light-sensitive films, facilitating image development through latent image formation upon exposure.^[6] Modern industrial applications encompass flame retardants, hydraulic fracturing fluids, and water treatment disinfectants, where bromide's oxidative stability and reactivity prove valuable, despite environmental regulations addressing bioaccumulation and ozonation byproducts.^[7]

Chemical Properties

Properties of the Bromide Ion

The bromide ion (Br⁻) possesses an ionic radius of 196 pm in six-coordinate environments, larger than that of the chloride ion (181 pm) but smaller than the iodide ion (220 pm), resulting in intermediate charge density and polarizing ability among the halide ions.^[8] This size influences its interactions in ionic lattices and solutions, with the atomic electronegativity of bromine at 2.96 on the Pauling scale contributing to the ion's moderate electron affinity. The standard reduction potential for the Br₂/2Br⁻ couple is +1.087 V versus the standard hydrogen electrode, positioned between the chloride couple (+1.36 V) and iodide couple (+0.535 V), indicating that Br⁻ is more readily oxidized to bromine than Cl⁻ but resists oxidation more than I⁻ under standard conditions.^[9] In aqueous solutions, Br⁻ exists primarily as a hydrated species, with hydration energy of approximately -337 kJ/mol, less exothermic than for Cl⁻ (-381 kJ/mol) due to its larger size and lower charge density.^[1] Solubility trends of bromide-containing ionic compounds follow Fajans' rules, where the larger, more polarizable Br⁻ promotes greater covalent character in bonds with small, highly charged cations compared to Cl⁻, often leading to reduced solubility in water relative to corresponding chlorides (e.g., with Ag⁺ or Pb²⁺).^[10] However, most alkali metal bromides exhibit high solubility in water, exceeding 100 g/100 mL at room temperature, governed by lattice energy and hydration effects. In organic solvents, Br⁻ shows moderate solubility in polar aprotic media due to its lipophilicity relative to smaller halides. Spectroscopic characterization of Br⁻ utilizes ⁷⁹Br (abundance 50.5%, I=3/2) and ⁸¹Br (49.3%, I=3/2) NMR, which display quadrupolar broadening in symmetric environments like aqueous solutions, with chemical shifts typically referenced near 0 ppm for free or symmetrically solvated ions relative to KBr standards.^[11] The wide chemical shift range (over 2000 ppm) for bromine nuclei allows distinction of ionic versus coordinated environments, though line widths often exceed 100 Hz for the bromide ion due to quadrupolar relaxation.^[12]

Properties of Bromide Compounds

Bromide salts of alkali metals are typically colorless to white crystalline solids with high melting and boiling points indicative of strong ionic bonding. Sodium bromide (NaBr) melts at 747 °C and boils at 1390 °C, while cesium bromide (CsBr) has a lower melting point of 636 °C and boils at 1300 °C, reflecting the decreasing lattice energy down the group due to increasing cation size.^[13]^[14]^[15] Alkali bromides are hygroscopic, absorbing atmospheric moisture, with lithium bromide (LiBr) and potassium bromide (KBr) exhibiting deliquescence under humid conditions, forming hydrates such as NaBr·2H₂O.^[13] Crystal structures of these salts vary with cation radius. NaBr and KBr crystallize in the rock salt (face-centered cubic) structure, where each cation is octahedrally coordinated to six bromide ions. In contrast, CsBr adopts the cesium chloride (body-centered cubic) structure, with eightfold coordination and a Cs–Br bond length of 3.75 Å, enabled by the larger cesium ion.^[16]^[17] Organic bromide compounds, such as bromoform (tribromomethane, CHBr₃), are often dense, volatile liquids at room temperature. Bromoform has a density of 2.89 g/cm³, exceeding that of water, and boils at 149.1 °C, contributing to its use in density gradient separations despite toxicity concerns.^[18] These compounds generally display greater density and lower volatility than analogous chlorides due to the heavier bromine atom, though many remain sufficiently volatile for applications requiring vapor-phase behavior; however, they can decompose thermally or photolytically, releasing bromine or hydrogen bromide.^[18]

Occurrence and Production

Natural Occurrence

Bromide ions occur naturally in seawater at an average concentration of approximately 65 mg/L, representing about 0.2% of the total dissolved salts and positioning bromide as the third most abundant halide ion after chloride (approximately 19,000 mg/L) and ahead of fluoride (1.3 mg/L).^[1]^[19] This distribution reflects the geochemical balance maintained through oceanic circulation and input from continental weathering and hydrothermal vents. In evaporite deposits formed by the evaporation of ancient seawater, bromide becomes concentrated in residual brines and associated minerals, as it is preferentially excluded from early-forming halite crystals, leading to enrichment in later-stage potash and magnesium salts.^[20] For instance, the Dead Sea, a hypersaline terminal lake, exhibits bromide levels of about 5.6 g/L due to extreme evaporation, far exceeding oceanic values.^[21] Similarly, brines within salt domes, such as those in the Gulf of Mexico region, show elevated bromide concentrations relative to surrounding formation waters, often exceeding 1,000 mg/L, attributable to dissolution of these evaporitic sequences.^[22] Trace quantities of bromide are cycled through biological systems via incorporation into organic matter in marine environments, where microorganisms and algae facilitate halogen exchange, resulting in natural organobromine compounds in sediments at levels correlating with organic carbon content (typically parts per million).^[23] This biogeochemical process contributes to bromide's global distribution but remains minor compared to abiotic oceanic and evaporitic reservoirs.^[24]

Commercial Production

Bromide for commercial use is obtained primarily through the large-scale extraction of bromine from natural brines, which is then converted into bromide salts such as sodium bromide (NaBr) and calcium bromide (CaBr₂) by reaction with appropriate bases. The principal sources are subsurface brines from the Smackover Formation in Arkansas, United States, containing 2,000–5,000 ppm bromide, and hypersaline surface waters of the Dead Sea, with bromide concentrations up to 5 g/L after prior extraction of sodium chloride and potash. Other significant sources include brines in China and Jordan, as well as bitterns—concentrated residual liquors—from seawater desalination or solar salt production, though these yield lower bromide levels around 65–200 ppm. Global bromine production, representing the bromide equivalent, reached approximately 600,000 metric tons in 2019, with the United States and Israel accounting for over half of output.^[25] The dominant industrial process begins with acidification of the brine using sulfuric acid to a pH of 3.5–4.5, followed by oxidation of bromide ions with chlorine gas according to the reaction 2Br⁻ + Cl₂ → Br₂ + 2Cl⁻. This liberates elemental bromine, which is stripped from the solution using countercurrent steam or air flow in packed towers at temperatures of 60–90°C, producing a bromine-enriched vapor. The vapor is then passed through condensers and subjected to fractional distillation under reduced pressure to purify the bromine to 99.8–99.9% assay, separating it from water, chlorine, and organic impurities. The purified bromine is subsequently reacted with sodium hydroxide or carbonate to form bromide salts, for example, Br₂ + 2NaOH → NaBr + NaOBr (followed by disproportionation to yield additional NaBr). This chlorination-steam stripping method, refined since the early 20th century, accounts for the majority of production due to its scalability and efficiency with concentrated brines.^[26]^[27] Electrolytic production, pioneered by Herbert H. Dow in 1891 using direct current to oxidize bromide at the anode (2Br⁻ → Br₂ + 2e⁻), was historically significant in Michigan and Arkansas but has largely been supplanted by chemical oxidation methods, which avoid high energy demands from electrolysis. Recovery from desalination bitterns involves similar chlorination and stripping but on a smaller scale, often as a coproduct to improve overall process economics. Cost factors include chlorine feedstock prices (typically $0.20–0.30/kg), energy for steaming and distillation (comprising 20–30% of operating costs), and brine transport; Dead Sea operations benefit from high bromide density, yielding lower unit costs of around $1–2/kg Br₂ equivalent versus $3–5/kg from dilute sources. Purity standards for bromide salts exceed 99% Br content, verified by titration and spectroscopy, ensuring suitability for industrial applications.^[28]^[29]^[30]

Synthesis and Reactions

Formation Mechanisms

Bromide ions (Br⁻) are generated primarily through the electrolytic dissociation of soluble bromide salts in aqueous media, a process driven by the favorable balance of lattice dissociation energy and ion solvation. For alkali metal bromides like potassium bromide (KBr), the reaction proceeds as KBr(s) ⇌ K⁺(aq) + Br⁻(aq), with near-complete dissociation due to high solubility exceeding 67 g/100 mL at 20°C and negligible ion-pairing in dilute solutions. Similarly, sodium bromide (NaBr) dissociates fully, as these salts behave as strong electrolytes with solubility products effectively approaching infinity under standard conditions, governed by Le Chatelier's principle favoring ionized states in polar solvents.^[31] Less soluble bromides, such as silver bromide (AgBr), exhibit limited dissociation per their Ksp of 5.4 × 10⁻¹³ at 25°C, but alkali and alkaline earth metal variants dominate natural and laboratory Br⁻ formation.^[32] A secondary pathway involves the hydrolysis of elemental bromine (Br₂), which equilibrates in water to yield bromide via disproportionation: Br₂(aq) + H₂O(l) ⇌ HOBr(aq) + HBr(aq). The hydrobromic acid (HBr) produced dissociates completely as a strong acid: HBr(aq) ⇌ H⁺(aq) + Br⁻(aq), introducing Br⁻ into solution. This reaction's equilibrium constant K₁ = [HOBr][H⁺][Br⁻]/[Br₂(aq)] is approximately 3.2–7.2 × 10⁻⁹ at 25°C, depending on ionic strength, shifting slightly toward products in acidic conditions but generally favoring undissociated Br₂.^[33] The process contributes modestly to Br⁻ concentrations in brominated aqueous systems, with overall bromide yield influenced by pH and competing oxidation. In natural aquatic environments, bromide forms through reductive pathways converting Br₂ or related species. Photochemical reduction under ultraviolet light decomposes Br₂ water, catalyzed by photolysis of hypobromous acid intermediates: 2HOBr → 2HBr + ½O₂, or net 2Br₂ + 2H₂O → 4HBr + O₂, yielding up to 57% conversion to HBr in dilute solutions exposed to light.^[34] Microbial reduction, primarily anaerobic bacteria utilizing organic substrates as electron donors, can similarly convert oxidized bromine (e.g., from hypobromite) to Br⁻ in sediments and bromide-rich waters, though rates vary with biomass and are better documented for bromate (BrO₃⁻) bioreduction with first-order constants of 0.3–0.8 L/(g biomass·h).^[35] These mechanisms maintain Br⁻ dominance in seawater at ~65 mg/L, countering transient Br₂ from oxidation processes.^[1]

Key Chemical Reactions

Bromide ions undergo oxidation to elemental bromine by oxidants with higher reduction potentials, such as chlorine. The reaction $2\mathrm{Br}^- + \mathrm{Cl}_2 \rightarrow \mathrm{Br}_2 + 2\mathrm{Cl}^- is thermodynamically spontaneous, with \Delta E^\circ \approx 0.29 V derived from the standard reduction potentials of \mathrm{Cl}_2/\mathrm{Cl}^- (1.36 V) and \mathrm{Br}_2/\mathrm{Br}^- (1.07 V versus SHE, favoring bromide displacement in mixed halide systems.^[36] Kinetically, this electron transfer proceeds rapidly in aqueous media, often approaching diffusion control, though influenced by pH and competing hydrolysis of \mathrm{Br}_2 to \mathrm{HOBr} and \mathrm{Br}^-.^[33] Similar oxidation occurs with ozone or persulfate, where bromide conversion to \mathrm{Br}_2 or bromate exhibits first-order kinetics with respect to oxidant concentration and activated by heat or UV, with activation energies around 50-100 kJ/mol depending on conditions.^[37] In nucleophilic substitution reactions, bromide serves both as a nucleophile and leaving group in organic halides. The Finkelstein reaction exemplifies halide exchange, converting alkyl chlorides or bromides to iodides via \mathrm{S_N}2 mechanism: e.g., \mathrm{RCl} + \mathrm{I}^- \rightarrow \mathrm{RI} + \mathrm{Cl}^- or reverse for bromides, driven by equilibrium shifts from differential solubility of sodium halides in acetone (NaCl precipitates, \mathrm{K} \approx 0.5-10 favoring iodide formation).^[38] For alkyl bromides as substrates, bromide departure is facile due to its polarizability, with rates following \mathrm{CH_3 > primary > secondary > tertiary} order and activation energies typically 80-100 kJ/mol, enhanced in polar aprotic solvents.^[39] Bromide forms coordination complexes with transition metals, acting as a ligand in tetrahedral or octahedral geometries, such as [\mathrm{FeBr_4}]^- or nickel(I)-bromide species like [\mathrm{NiBr(PR_3)_3}], stabilized by \sigma-donation and \pi-acceptance, with formation constants influenced by metal oxidation state and counterions.^[40] In catalysis, bromide ions or salts promote palladium-mediated cross-couplings, including the Heck reaction, where additives like tetrabutylammonium bromide facilitate chemoselective arylation of alkenes by aryl bromides through phase-transfer effects and stabilization of Pd(0)/Pd(II) cycles, improving turnover frequencies up to 10^4 mol^{-1} under mild conditions.^[41] These roles leverage bromide's intermediate electronegativity, enabling reversible binding with \Delta H \approx -20 to -50 kJ/mol for complexation.^[42]

Industrial Applications

Flame Retardants and Materials

Brominated compounds, including polybrominated diphenyl ethers (PBDEs) such as decabromodiphenyl ether (decaBDE) and hexabromocyclododecane (HBCD), serve as additive flame retardants in polymers for electronics housings, circuit boards, and textiles.^[43] ^[44] These materials release bromine radicals upon heating, which interfere with the gas-phase combustion chain reactions by scavenging hydrogen and hydroxyl radicals, thus suppressing flame propagation and reducing peak heat release rates.^[45] This mechanism enables treated products to achieve high flammability resistance, such as UL 94 V-0 ratings, providing critical escape time during fires in high-risk applications like consumer electronics.^[45] Empirical data underscore their effectiveness in fire prevention: for instance, brominated flame retardants in television enclosures are estimated to save approximately 190 lives per year in the United States by delaying ignition and limiting fire spread.^[46] Broader assessments indicate that flame retardants, including brominated variants, contribute to averting substantial property damage, with U.S. structure fires alone causing over $10 billion in losses in 2001 prior to widespread adoption enhancements.^[47] However, regulatory scrutiny has intensified due to evidence of persistence and bioaccumulation; pentaBDE and octaBDE commercial mixtures were restricted in the European Union starting in 2004, followed by their listing under the Stockholm Convention in 2009, which mandates global phase-out except for specific exemptions.^[48] HBCD faced similar listing in 2013, prompting industry shifts amid debates over whether bioaccumulation risks outweigh fire safety gains, with critics from environmental groups emphasizing long-range transport while proponents cite life-saving data from peer-reviewed fire modeling.^[49] Phosphorus-based alternatives, such as organophosphates like resorcinol bis(diphenylphosphate), operate primarily in the condensed phase by promoting char formation and reducing fuel volatilization, offering halogen-free options for similar applications.^[50] ^[51] Comparative testing shows these compounds can achieve comparable limiting oxygen index values in polyolefins but often necessitate 20-50% higher loadings than brominated equivalents to match heat release suppression in styrenic polymers, potentially compromising mechanical properties or cost-effectiveness.^[52] In electronics, brominated systems retain advantages for vapor-phase inhibition, though phosphorus variants have gained traction post-restrictions, with lifecycle analyses indicating trade-offs in efficacy versus lower persistence.^[53] Ongoing research prioritizes hybrid formulations to balance these metrics without relying on first-generation bromides.

Water Treatment and Disinfectants

Bromine-based disinfectants, primarily in the form of hypobromous acid (HOBr) or sodium hypobromite (NaOBr), are commonly employed for sanitizing swimming pools and spas, where they offer advantages over chlorine in certain conditions.^[54] Sodium bromide is typically added to the water and oxidized—often by chlorine or monopersulfate—to generate HOBr, the active disinfecting species.^[55] This approach maintains effective sanitation levels, particularly in alkaline environments (pH 7.0–8.5), where HOBr remains predominantly undissociated and retains greater biocidal activity compared to hypochlorous acid (HOCl), which loses efficacy above pH 7.5.^[56] ^[57] HOBr demonstrates superior inactivation kinetics against certain pathogens relative to chlorine, including protozoans like Cryptosporidium parvum oocysts, which are notoriously resistant to chlorination. At concentrations around 5 mg/L as Br₂, bromine achieves approximately 0.6 log (74%) reduction in C. parvum oocyst infectivity after 300 minutes (CT value of 1166 mg·min/L), outperforming chlorine under similar conditions where chlorine yields negligible inactivation.^[58] This makes bromine preferable for recreational water systems prone to protozoan contamination, though extended contact times are required for substantial log reductions.^[59] Despite these benefits, bromination generates disinfection byproducts (DBPs) via reactions between HOBr and natural organic matter or bromide ions, including bromoform, dibromochloromethane, and brominated haloacetic acids, which exhibit higher cytotoxicity, genotoxicity, and carcinogenicity than their chlorinated analogs.^[60] ^[61] In advanced treatments like ozonation of bromide-containing source waters, bromide oxidizes to bromate (BrO₃⁻), a probable human carcinogen regulated by the U.S. EPA at a maximum contaminant level of 10 μg/L (ppb) to minimize cancer risks.^[62] ^[63] Empirical toxicity indices, such as those from bioassays, confirm brominated DBPs contribute disproportionately to overall DBP-associated health risks, often 2–10 times more potent than chlorinated species on a molar basis.^[64] These factors necessitate careful bromide dosing and byproduct monitoring in treatment processes to balance disinfection efficacy against elevated toxicity profiles.^[65]

Other Industrial Uses

Silver bromide (AgBr) is utilized in photographic emulsions for traditional film and paper due to its photosensitivity, where exposure to light reduces silver ions to metallic silver clusters, forming a latent image that is developed chemically.^[66] This technology, introduced in the gelatin dry plate process in the 1870s, dominated image capture through the 20th century, with global silver consumption for photography peaking at over 200 million ounces annually in the 1990s.^[67] Production declined precipitously after 2000 as digital cameras supplanted film, reducing silver halide demand by more than 90% by the 2010s and relegating it to niche analog and specialty applications.^[68] Bromide compounds, notably calcium bromide (CaBr₂), function as high-density clear brines in drilling, completion, and workover fluids for oil and gas wells, including shale formations accessed via hydraulic fracturing.^[69] These brines provide densities up to 14.7 pounds per gallon (1.76 g/cm³) to counter high formation pressures, prevent fluid influx, and maintain wellbore stability under elevated temperatures and pressures common in unconventional reservoirs.^[70] Certain hydraulic fracturing formulations include bromide salts, such as in biocide additives, to support fluid performance amid the chemical demands of proppant transport and fracture propagation.^[71] In pharmaceutical manufacturing, bromide compounds enable bromination reactions essential for synthesizing intermediates, where bromine acts as an electrophile to functionalize aromatic rings or alkyl chains, yielding precursors for active ingredients.^[3] Catalysts like copper(II) bromide facilitate selective α-bromination of substrates such as benzylic esters, streamlining one-pot processes that reduce energy use and improve yields in drug production.^[72] Bromine-based reagents are incorporated in up to 10% of organic synthesis steps for pharmaceuticals, prized for their precision in introducing reactive handles for subsequent cross-coupling or substitution.^[73]

Biological Role and Biochemistry

Biochemical Functions

In marine algae, vanadium bromoperoxidase (VBrPO) enzymes utilize bromide ions as a substrate in the presence of hydrogen peroxide to catalyze the halogenation of organic compounds, producing brominated defense metabolites that deter herbivores and pathogens.^[74] These enzymes facilitate the two-electron oxidation of bromide, generating reactive brominating intermediates that incorporate into secondary metabolites essential for algal survival in competitive marine environments. Bromide acts as a competitive inhibitor of iodide uptake in the thyroid gland via the sodium-iodide symporter (NIS), potentially disrupting iodine-dependent hormone synthesis at elevated concentrations.^[75] This interference occurs because bromide shares structural similarity with iodide, allowing it to bind the symporter and reduce iodide transport affinity.^[76] In mammalian systems, eosinophil peroxidase (EPO), a heme-containing haloperoxidase, incorporates trace bromide to produce hypobromous acid (HOBr) from hydrogen peroxide, contributing to antimicrobial defense in innate immune responses.^[77] EPO preferentially oxidizes bromide over chloride under physiological conditions, yielding HOBr that targets microbial pathogens and modulates inflammation in eosinophil-rich tissues.^[78]

Role as Substrate and Cofactor

Bromide functions as a substrate for lactoperoxidase (LPO), a heme-containing enzyme present in saliva, milk, and other exocrine secretions, where it is oxidized by LPO-generated compound I in the presence of hydrogen peroxide to form hypobromous acid (HOBr).^[79] This HOBr acts as a potent oxidant with antibacterial and antifungal properties, contributing to innate immune defense against pathogens in mucosal environments, though thiocyanate is the preferred substrate under typical physiological conditions.^[80] Similar halide oxidation occurs via eosinophil peroxidase and myeloperoxidase in inflammatory responses, underscoring bromide's role in peroxidase-mediated halogenation for microbial killing.^[81] In marine ecosystems, bromide serves as a substrate for vanadium-dependent bromoperoxidases in organisms such as sponges and algae, facilitating the regioselective bromination of tyrosine residues to produce bromotyrosine alkaloids and other secondary metabolites.^[82] These compounds, including derivatives like aerothionin and homoaerothionin, exhibit diverse bioactivities such as antimicrobial and cytotoxic effects, with bromination typically occurring at the ortho position of the phenolic ring.^[83] The process relies on bromide's availability in seawater, highlighting its incorporation into non-ribosomal peptide synthesis pathways in invertebrate natural products.^[84] Bromide is also a required substrate for peroxidasin, an extracellular heme peroxidase that generates HOBr to catalyze sulfilimine (-S=N-) cross-link formation between methionine and hydroxylysine residues in collagen IV triple helices.^[85] This modification stabilizes basement membrane scaffolds essential for tissue development and integrity across animals, from fruit flies to mammals; bromide deficiency disrupts this process, confirming its biochemical necessity despite not being classified as a traditional dietary essential.^[86] Human dietary intake of bromide, typically 2–8 mg per day from sources including grains, nuts, and seafood, supports these trace roles without established deficiency syndromes under normal conditions.^[87]

Medical and Veterinary Uses

Historical Uses as Sedative and Antiepileptic

Potassium bromide was introduced as a treatment for epilepsy in 1857 by Sir Charles Locock, physician to Queen Victoria, who reported its efficacy in reducing seizures in 15 cases of what he described as "hysterical epilepsy" in young women during a discussion at the Royal Medical and Chirurgical Society.^[88] Locock's observations followed earlier limited trials, including one in 1856, and marked the first pharmacological agent demonstrated to suppress epileptic convulsions reliably, supplanting prior ineffective remedies like bloodletting or dietary restrictions.^[89] Historical clinical records from the era documented seizure frequency reductions of up to 80% in responsive patients at doses of 3-5 grams daily, establishing bromides as the standard antiepileptic therapy for over half a century.^[90] Beyond epilepsy, bromides gained prominence as sedatives in the late 19th century, prescribed for hysteria, anxiety, insomnia, and nervous disorders, with potassium bromide often administered in tonics or elixirs at 1-3 grams per dose.^[91] Their calming effects stemmed from empirical observations of behavioral suppression, leading to widespread adoption in psychiatric and general practice; by the early 1900s, annual consumption in the United States exceeded 100 tons, reflecting over-the-counter availability in patent medicines like Bromo-Seltzer for headache and sedation.^[92] Therapeutic blood levels of 800-1500 mg/L correlated with sedation, but slow excretion (half-life of 12 days) necessitated careful dosing to avoid accumulation.^[90] Bromides' dominance persisted into the mid-20th century despite reports of toxicity, including bromism characterized by acneiform rashes, lethargy, and psychosis at levels above 1500 mg/L, which affected up to 10% of long-term users in institutional settings.^[91] Replacement began with phenobarbital's introduction in 1912, which offered comparable efficacy with faster clearance, followed by phenytoin's commercialization in 1938, both exhibiting wider therapeutic windows and reduced chronic side effects.^[93] By the 1950s, bromides were largely supplanted in favor of these alternatives due to their narrow safety margin rather than lack of anticonvulsant potency, though they remained available over-the-counter until FDA restrictions in the 1960s and 1970s curtailed non-prescription sedative formulations amid toxicity concerns.^[92]^[90]

Current Therapeutic Applications

Potassium bromide is employed as an antiepileptic drug in veterinary medicine, primarily for dogs with idiopathic epilepsy inadequately controlled by phenobarbital. As adjunctive therapy, typical dosages range from 20-40 mg/kg/day orally, achieving therapeutic serum concentrations of 800-3,000 µg/mL after 2-3 weeks, though loading doses of 400-600 mg/kg over several days may accelerate onset for urgent cases.^[94]^[95] In monotherapy, it controls seizures in approximately 52% of cases when used as first-line treatment, with ongoing utility demonstrated in canine epilepsy management for over three decades per 2024 veterinary reviews.^[90] The U.S. FDA conditionally approved KBroVet-CA1 chewable tablets in January 2021 specifically for seizure control in dogs with idiopathic epilepsy.^[96] Human applications of bromide are restricted to exceptional circumstances, such as adjunctive treatment for intractable epilepsy syndromes including certain myoclonic seizures refractory to conventional antiseizure medications. Institutions like Great Ormond Street Hospital in the UK continue to utilize bromide formulations for pediatric patients with severe, drug-resistant epilepsy where other therapies fail.^[97] Benzalkonium bromide serves as a quaternary ammonium biocide in therapeutic formulations, functioning as a preservative in ophthalmic solutions, nasal sprays, and topical medications to prevent microbial contamination, and as an antiseptic for skin, mucous membrane, and wound disinfection at concentrations of 0.01-0.1%.^[98]^[99] Its cationic surfactant properties disrupt bacterial cell membranes, conferring broad-spectrum antimicrobial activity suitable for these applications.^[100]

Mechanisms of Action

Bromide ions primarily mediate central nervous system (CNS) depression and anticonvulsant effects by substituting for chloride ions in neuronal chloride channels associated with GABA_A receptors, leading to enhanced inhibitory postsynaptic potentials. This substitution facilitates bromide influx during GABA binding, resulting in greater neuronal hyperpolarization than chloride alone due to bromide's higher permeability and intracellular accumulation, which reduces excitability and stabilizes membranes against seizure propagation.^[90] ^[101] Therapeutic plasma concentrations of 750–1500 mg/L (equivalent to 10–20 mM) achieve this by potentiating GABA-activated chloride currents by 28–36%, akin to the inhibitory enhancement by benzodiazepines but with slower onset owing to reliance on ion equilibration rather than rapid allosteric modulation.^[102] ^[103] In anticonvulsant applications, bromide further reduces neuronal firing by interfering with chloride transport and amplifying GABA-mediated inhibition, elevating the seizure threshold without directly altering voltage-gated sodium channels.^[104] This mechanism underpins its historical use in refractory epilepsy, where steady-state levels correlate with reduced seizure frequency.^[105] For antimicrobial activity in therapeutic contexts, bromide acts as a substrate for heme peroxidases such as myeloperoxidase or eosinophil peroxidase, which oxidize it using hydrogen peroxide to form hypobromous acid (HOBr). HOBr then selectively oxidizes microbial proteins, particularly sulfhydryl and tryptophan residues, disrupting enzymatic function and cell wall integrity in pathogens.^[106] This oxidative pathway contributes to bromide's role in certain veterinary disinfectants or innate-like antimicrobial strategies, though it requires enzymatic activation and is less prominent than in CNS applications.^[107]

Health Effects and Toxicity

Bromism and Acute Toxicity

Bromism, also known as bromide intoxication, arises from chronic accumulation of bromide ions (Br⁻) in the body, primarily due to prolonged ingestion of bromide-containing compounds, leading to plasma concentrations exceeding 1000 mg/L.^[108] Symptoms include dermatological manifestations such as acneiform rash (bromoderma), characterized by pustular lesions resembling acne but often more severe and widespread; neurological effects like ataxia, tremors, slurred speech, and hallucinations; and psychiatric disturbances including psychosis with delusions and apathy.^[109] These arise mechanistically from Br⁻ interference with neuronal chloride channels, mimicking inhibitory neurotransmission and disrupting GABAergic signaling, compounded by its competitive inhibition of chloride transport.^[110] Bromide's biological half-life averages 9–12 days in humans, prolonged by low dietary chloride intake which reduces renal excretion via shared tubular reabsorption pathways, with clearance rates around 26 mL/kg/day under normal conditions.^[111] Diagnosis involves measuring serum bromide levels directly (via ion-selective electrodes or chromatography), alongside laboratory findings of pseudohyperchloremia—where bromide is misread as chloride by automated analyzers—and a negative anion gap (typically below -10 mEq/L) due to overestimation of serum chloride.^[112] Acute bromide toxicity from high-dose ingestion manifests initially with gastrointestinal distress, including nausea, vomiting, abdominal pain, and diarrhea, progressing to central nervous system depression, coma, or respiratory failure in severe cases.^[113] Mechanistically, rapid absorption overwhelms renal clearance, causing osmotic effects and direct cellular toxicity, with laboratory hallmarks mirroring chronic cases: hyperchloremia artifact and negative anion gap.^[114] In animal models, the oral LD50 for sodium bromide in rats is approximately 3.5 g/kg, indicating relatively low acute lethality compared to other halides, though human thresholds vary with dose rate and comorbidities.^[115] A notable 2025 case involved a 60-year-old man who, following dietary advice from an AI chatbot to substitute table salt with sodium bromide for purported health benefits, developed bromism after three months of use, presenting with hallucinations, ataxia, and bromide levels of 1,200 mg/L; symptoms resolved after cessation and supportive care.^[116] Treatment for both acute and bromism cases centers on discontinuing exposure and enhancing elimination through intravenous saline diuresis, which exploits bromide's chloride competition to accelerate urinary excretion, reducing half-life to 2–3 days; adjuncts may include ammonium chloride to further promote diuresis without exacerbating dehydration.^[110] Hemodialysis is reserved for severe cases with renal impairment or refractory symptoms, as bromide is dialyzable.^[117] Prognosis is favorable with prompt intervention, as symptoms correlate inversely with declining bromide levels, though residual neurological effects can persist in prolonged exposures.^[109]

Chronic Exposure Risks

Chronic exposure to bromide ions (Br⁻) through dietary sources or drinking water primarily poses risks via competitive inhibition of iodide (I⁻) uptake in the thyroid gland, potentially leading to altered thyroid hormone homeostasis.^[76]^[75] This mechanism substitutes Br⁻ for I⁻ at the sodium-iodide symporter, creating relative iodine insufficiency that impairs thyroxine (T4) and triiodothyronine (T3) synthesis in animal models.^[118] In humans, empirical evidence from low-level chronic exposure remains limited, with no robust epidemiological studies demonstrating clear thyroid dysfunction at typical environmental concentrations below 10 mg/L in water.^[75] The European Food Safety Authority (EFSA) assessed bromide toxicity in 2025, identifying thyroid disruption as the critical endpoint, with potential neurodevelopmental effects in offspring from maternal exposure in experimental animals at high feed levels exceeding 100 mg/kg body weight per day.^[75] However, human data indicate no established neurodevelopmental risks at dietary exposures aligned with current maximum residue levels in food, emphasizing the need for adequate iodine intake to mitigate competitive effects.^[75] Central nervous system alterations, such as subtle behavioral changes, have been observed in rodents under chronic dosing but lack confirmation in human cohorts.^[75] Bromate (BrO₃⁻), a bromide-derived disinfection byproduct in ozonated water, presents carcinogenic concerns based on rodent studies showing renal and thyroid tumors at doses above 5 mg/kg body weight per day.^[119] The International Agency for Research on Cancer (IARC) classifies bromate as possibly carcinogenic to humans (Group 2B), citing sufficient animal evidence but inadequate human data, with no conclusive links to cancer at concentrations below the World Health Organization guideline of 0.01 mg/L.^[120]^[121] In livestock, chronic dietary bromide exposure induces dose-dependent effects, including growth inhibition and reduced feed efficiency in broilers at concentrations exceeding 200 ppm in feed, alongside hypothyroidism and diminished milk or egg production in ruminants and poultry.^[122]^[75] These outcomes stem from thyroid-mediated metabolic disruptions, with field observations in bromide-contaminated regions confirming lower weight gains and reproductive performance without acute toxicity signs.^[123] EFSA notes that such risks are manageable below established feed tolerances, prioritizing iodine supplementation in affected herds.^[75]

Debunking Common Myths

One persistent myth alleges that bromide salts were routinely added to the tea or rations of British soldiers during World War I to suppress sexual libido and maintain discipline. This claim lacks historical documentation, with analyses attributing it to folklore amplified by bromide's known sedative side effects rather than archival evidence of deliberate dosing. A 2009 review by science communicator Dr. Karl Kruszelnicki examined purported references, including literary accounts, and found them anecdotal and unverifiable, concluding no systematic military practice occurred.^[124] ^[125] Bromide therapy for sedation and epilepsy is sometimes dismissed as an unsubstantiated 19th-century fad or quackery, ignoring its demonstrated clinical utility. Potassium bromide, introduced in 1857 by Sir Charles Locock, proved effective as the first reliable anticonvulsant, reducing seizure frequency in patients through mechanisms involving neuronal chloride channel modulation, as validated in early observational trials and subsequent use until the 20th century. Its phase-out stemmed from chronic toxicity risks like bromism and the development of less burdensome alternatives such as phenobarbital in 1912, not inefficacy or pseudoscience.^[90] ^[126] ^[127] Exaggerated fears of bromide as an ubiquitous environmental toxin often overlook its natural prevalence and low acute hazard in unmodified forms. Seawater typically contains 65 mg/L of bromide ion—orders of magnitude higher than inland freshwater—yet sustains diverse marine life without bromide-attributed die-offs, reflecting evolutionary adaptation and the ion's minimal direct toxicity at ambient levels. Human and ecological risks are confined to elevated anthropogenic inputs forming reactive byproducts during disinfection, which are mitigable through treatment adjustments rather than inherent bromide peril.^[2] ^[128]

Environmental Impact

Sources of Environmental Bromide

Bromide ions (Br⁻) enter the environment primarily from natural oceanic sources, where seawater contains an average concentration of approximately 65 mg/L, leading to inputs via coastal runoff, aerosolization, and riverine transport to inland waters.^[129]^[128] Volcanic activity contributes gaseous hydrogen bromide (HBr) emissions, which oxidize in plumes to form bromide species that deposit atmospherically or through wet scavenging, with detectable BrO levels observed in eruptions like those at Mount Etna.^[130] These natural fluxes maintain baseline environmental bromide levels, though quantitative global estimates for volcanic bromide deposition remain limited. Anthropogenic sources dominate localized elevations, particularly from industrial bromine extraction processes that utilize bromide-rich brines and seawater, generating effluents with residual Br⁻ during chlorine oxidation steps.^[26] In hypersaline bodies like the Dead Sea, where bromide concentrations reach 5–12 g/L—far exceeding oceanic averages—large-scale extraction for bromine production has intensified local cycling, with operations since the 1950s processing thousands of tons annually and potentially releasing process waters.^[131]^[132] Energy extraction activities, including hydraulic fracturing, introduce bromide through fluids recycled from produced waters containing elevated Br⁻ from subsurface formations, contributing to surface water contamination.^[133] Waste management practices, such as landfill leachates from disposed electronics and plastics, leach bromide from brominated flame retardants (BFRs) like polybrominated diphenyl ethers (PBDEs), with concentrations varying by landfill age and liners but often higher in modern, lined facilities due to retained organics.^[134] These inputs, alongside emissions from pesticide residues and coal combustion, amplify bromide in terrestrial and aquatic compartments beyond natural baselines.^[128]

Formation of Byproducts in Water

Bromate ion (BrO₃⁻) forms during ozonation of bromide-containing waters via a multi-step oxidation pathway initiated by direct reaction of ozone (O₃) with bromide (Br⁻) to produce hypobromite (OBr⁻), followed by further oxidation involving hydroxyl radicals (•OH) generated from O₃ decomposition.^[62] The yield of bromate rises significantly at pH values exceeding 7, as higher pH promotes O₃ decay to •OH and shifts the HOBr/OBr⁻ equilibrium toward the more reactive OBr⁻, accelerating the final oxidation step to BrO₃⁻; for instance, in Seine River water with 60 μg/L Br⁻, bromate levels increased markedly above neutral pH.^[135] Kinetic models indicate second-order dependence on Br⁻ concentration and O₃ dose, with rate constants for Br⁻ to HOBr/OBr⁻ around 1.8 × 10⁶ M⁻¹ s⁻¹ and subsequent steps limited by •OH scavenging in natural waters.^[136] Brominated disinfection byproducts (Br-DBPs), such as haloacetonitriles (HANs) and halonitromethanes (HNMs), demonstrate elevated cytotoxicity and genotoxicity relative to chlorinated counterparts, with 2023 assays showing Br-HANs and Br-HNMs requiring lower concentrations (e.g., LC₅₀ values 2–10 times smaller in mammalian cell lines) to induce equivalent cell death or DNA damage.^[137] These Br-DBPs form preferentially when Br⁻ is present during chlorination or ozonation, incorporating into organic precursors like natural organic matter, and contribute disproportionately to overall mixture toxicity despite lower molar yields.^[138] UV/chloramine advanced oxidation processes enhance Br⁻ incorporation into DBPs by generating reactive bromine species (e.g., HOBr from Br⁻ oxidation by chloramine radicals), boosting HNM formation from amine precursors and elevating genotoxicity indices by up to 20–50% in bromide-spiked waters.^[139] This occurs via UV-induced homolysis of chloramine, producing •Cl and •NH₂ radicals that abstract Br⁻, followed by recombination pathways favoring brominated N-DBPs over chlorinated ones.^[140] Strategies to mitigate byproduct formation include ammonia addition prior to ozonation, which competes with Br⁻ for •OH via formation of bromamines and reduces bromate yields by 50–70% without fully eliminating it, and granular activated carbon adsorption post-treatment, achieving >90% bromate removal in bench-scale tests on ozonated effluents.^[135]^[141] These approaches target kinetic suppression or physical removal, respectively, while preserving disinfection efficacy.^[142]

Ecological and Regulatory Considerations

Bromide ions are ubiquitous in natural waters, with seawater concentrations typically ranging from 65 to 80 mg/L and freshwater levels generally below 0.5 mg/L, levels to which aquatic organisms are adapted without evident population-level harm.^[143] Elevated bromide from anthropogenic sources, such as industrial discharges or seawater intrusion into coastal aquifers, can indirectly affect ecosystems by facilitating bromate formation during ozonation or chlorination of drinking water, with bromate showing toxicity to sensitive aquatic species at concentrations around 3 mg/L.^[135] Direct toxicity of inorganic bromide salts to fish remains low, with 96-hour LC50 values often exceeding typical exposure scenarios and far above natural baselines.^[144] Regulatory measures have effectively mitigated bromide-related ecological risks, particularly through controls on brominated disinfection byproducts and persistent organic pollutants. The U.S. EPA established a maximum contaminant level of 10 μg/L for bromate in drinking water under the Stage 1 Disinfectants and Disinfection Byproducts Rule in 1998, aiming to curb formation from bromide-ozone reactions while balancing disinfection needs.^[145] Similarly, the EU Drinking Water Directive sets a 10 μg/L limit for bromate, enforced since 2007 revisions to prior standards.^[146] The EU's 2004 phase-out of penta- and octa-polybrominated diphenyl ethers (PBDEs) under the Restriction of Hazardous Substances Directive and subsequent Stockholm Convention listings reduced atmospheric emissions, which peaked at approximately 10 tonnes/year for decaBDE in 2004, leading to measurable declines in PBDE bioaccumulation in European sediments and wildlife by the 2010s.^[147] Ongoing policy debates weigh bromide compound restrictions against their utility in fire retardants, where brominated variants offer cost-effective suppression of flame spread and ignition, potentially averting greater environmental costs from uncontrolled fires.^[148] These measures have achieved risk reductions without documented cases of ecosystem-wide collapse attributable solely to bromide exposure, underscoring a pragmatic balance between precaution and practical benefits.^[149]

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Bromide: the good, the bad, and the ugly of the oldest antiseizure ...
Bromide has now been successfully used as an ASM in the treatment of canine epilepsy for more than three decades (14, 16). The aim of this paper is to give a ...
[95]
Potassium Bromide - an overview | ScienceDirect Topics
If more rapid seizure control is necessary, an initial dose of 400 to 600 mg/kg, usually divided over a 2- to 3-day period, can be administered. Potassium ...
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Conditional Approval of Potassium Bromide for Dogs - FDA
Feb 12, 2021 · In January 2021, FDA conditionally approved KBroVet-CA1 (potassium bromide chewable tablets) to control seizures in dogs with idiopathic epilepsy.<|separator|>
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Bromide for epilepsy | Great Ormond Street Hospital
Bromide is a type of medication used to treat severe epilepsy, particularly causing myoclonic seizures. Bromide comes in two formulations: triple bromide ...
[98]
Benzalkonium: Uses, Interactions, Mechanism of Action - DrugBank
Benzalkonium is an antiseptic agent used as a preservative in medications or as a disinfectant in cleaning products.
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Benzalkonium bromide solution - Echemi
Used for disinfection of skin, mucous membranes and small wounds. Usage and Dosage. Use 0.01% solution for face disinfection, 0.1% solution for skin and mucous ...
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Topical effect of benzalkonium bromide on wound healing and ... - NIH
Jan 29, 2021 · Benzalkonium bromide (BB) has been widely used as a skin antiseptic for wound management. However, BB had proinflammation and reactive oxygen ...
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Bromide, in the therapeutic concentration, enhances GABA ...
These findings showed that the currents were composed of chloride flux through GABAA receptor-coupled channels. ... Mechanisms of action of anticonvulsants.
[102]
Bromide, in the therapeutic concentration, enhances GABA ...
Bromide enhances GABA-activated currents in neurons, with therapeutic concentrations of 10-20 mM enhancing currents 1.28- and 1.36-fold, respectively.
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International Veterinary Epilepsy Task Force consensus proposal
Aug 28, 2015 · Therapeutic ranges have been reported as approximately 1000 mg/l ... Hepatic cirrhosis associated with long-term anticonvulsant drug therapy in ...<|separator|>
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Anticonvulsants for Treatment of Animals - Merck Veterinary Manual
Bromide appears to stabilize neuronal cell membranes by interfering with membrane transport of chloride and by potentiating the effect of gamma-aminobutyric ...
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Use and monitoring of bromides in epilepsy treatment - ScienceDirect
This review provides an update on the mechanism of action, efficacy, pharmacokinetics, dose, and adverse effects of bromides.
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Peroxidase-mediated bromination of unsaturated fatty acids to form ...
Eosinophil peroxidase and myeloperoxidase (MPO) catalyze the oxidation of bromide by hydrogen peroxide to produce hypobromous acid (HOBr).
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Reactivity of BrCl, Br2, BrOCl, Br2O, and HOBr Toward ...
Jan 16, 2013 · HOBr, formed via oxidation of bromide by free available chlorine (FAC), is frequently assumed to be the sole species responsible for generating ...
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Bromide toxicosis (bromism) secondary to a decreased chloride ...
Jul 22, 2021 · As a consequence, the rate of renal elimination of bromide varies directly with chloride intake: high dietary chloride will increase bromide ...
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Case Report and Canadian Review of Bromide Intoxication
May 18, 2020 · Diagnosis is critical as toxicity may be completely reversible with cessation of bromide ingestion and medical management. Explore related ...Missing: distress | Show results with:distress
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Bromine Derivative - an overview | ScienceDirect Topics
The elimination half-life of bromide is 7 to 12 days; this half-life is increased with a salt-deficient diet. Average renal bromide clearance is about 26 mL/kg ...
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https://accessmedicine.mhmedical.com/content.aspx?bookid=2284&sectionid=248383784
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Unexplained Bromide Toxicity Presenting as Hyperchloremia and a ...
Mar 16, 2023 · Keywords: altered mental state, electrolyte imbalance, hyperchloremia, negative anion gap, bromide toxicity ... Toxic effects of bromide ...Missing: GI distress
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Acute Bromide Intoxication in a Patient with Preserved Renal Function
Jul 25, 2025 · Conclusions It is important to recognize that hyperchloremia with a negative anion gap strongly suggests bromide intoxication, and that bromide ...Missing: distress | Show results with:distress<|separator|>
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Spurious Hyperchloremia and Negative Anion Gap in a Child with ...
Apart from bromide ingestion, iodide, lithium intoxication, and monoclonal proteinemia can give rise to negative anion gap [11]. Treatment with aggressive ...Missing: distress | Show results with:distress
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Toxicity of sodium bromide in rats: effects on endocrine system and ...
Bromide has a low acute oral toxicity, with LD50 values in rodents ranging from 3500 to 7000 mg/kg body weight. It is rapidly absorbed and steady-state ...Missing: treatment diuresis
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Man develops rare condition after ChatGPT query over stopping ...
Aug 12, 2025 · US medical journal article about 60-year-old with bromism warns against using AI app for health information.Missing: self- | Show results with:self-
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Sodium bromide | CAS#:7647-15-6 | Chemsrc
Aug 19, 2025 · Treatment includes hydration, mild diuresis, and possible hemodialysis. ... CAS# 7647-15-6: Oral, mouse: LD50 = 7 gm/kg; Oral, rat: LD50 = 3500 mg ...
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Effects of the Environment, Chemicals and Drugs on Thyroid Function
Sep 27, 2016 · Bromine is concentrated by the thyroid and interferes with the thyroidal 131I uptake in animals99,99a and humans, possibly by competitive ...
[119]
Potassium bromate - NCBI Bookshelf - NCBI - NIH
There is inadequate evidence in humans for the carcinogenicity of potassium bromate. There is sufficient evidence in experimental animals for the ...
[120]
Potassium Bromate (IARC Summary & Evaluation, Volume 73, 1999)
Sep 30, 1999 · There is inadequate evidence in humans for the carcinogenicity of potassium bromate. There is sufficient evidence in experimental animals ...
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[PDF] IARC has concluded that although there is inadequate evidence of ...
Bromate is mutagenic both in vitro and in vivo. At this time, there is not sufficient evidence to conclude as to the mode of carcinogenic action for bromate.
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Effect of Bromide on Livestock Development: A Review - Qeios
Jul 5, 2024 · Inorganic Br- was shown to influence broiler growth and feed efficiency negatively even after short-term exposure to a maximum concentration of ...
[123]
Effect of Bromide on Livestock Development: A Review
Jul 5, 2024 · Chronic and acute exposure to Br- in groundwater can induce negative consequences, which include hypothyroidism, reduced production and Br- ...
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Military myth puts lead in bromide's pencil - Dr Karl - ABC News
Jun 29, 2009 · The author Paul Ferris refers to the use of bromide to reduce the sexual libido of soldiers. But once again, it's not true.
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Who's afraid of bromine? - BBC News
Sep 27, 2014 · The earliest use of bromine was in medicines. Some bromide salts, notably potassium bromide, were found to be natural sedatives, and were ...
[126]
Highights in the History of Epilepsy: The Last 200 Years
Aug 24, 2014 · In 1857, Sir Locock (1799–1875) discovered the anticonvulsant and sedative traits of potassium bromide and began treating his patients.
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The rise and fall of bromide therapy in epilepsy. - Semantic Scholar
An examination of the rise and fall of bromides as antiepileptics demonstrates, in relatively slow-motion, what can occur when a useful drug is introduced ...
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Bromine contamination and risk management in terrestrial and ...
Immobilization using adsorbents is a practical approach for Br remediation. Br remediation via phyto- and microbial means can be environmentally sustainable.
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Review Bromine contamination and risk management in terrestrial ...
May 5, 2024 · High Br levels in the environment are toxic to ecosystems and human health. •. Br in drinking water plants forms toxic brominated disinfection ...
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Reactive bromine in volcanic plumes confines the emission ...
Apr 30, 2025 · Many volcanic plumes contain high levels of bromine monoxide (BrO), which is produced by atmospheric oxidation of magmatic hydrogen bromide (HBr) emissions.
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Recovery of bromide for bromine extraction - ScienceDirect.com
The Dead Sea has Br− concentrations of 5–12 g/L and is the world's largest and most significant source of industrial Br2 production [20,21]. Other major sources ...
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[PDF] Bromine from the Dead SeaBromine from the Dead Sea
The average salt concentration in Dead Sea water is approximately 30% (about. 310°g/liter) while in regular seawater the concentration is approximately 3-4%. ( ...
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Bromide in Surface Waters - Capps Lab at UGA
... bromide (Kolker et al. 2006). The highest natural concentrations of bromide are found in seawater (66-68 mg/L), shale geologic formations (24 mg/kg), and ...
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Brominated flame retardants and perfluoroalkyl substances in ...
Dec 10, 2019 · We reveal that leachate from newer landfills fitted with impervious liners contain significantly higher concentrations of some PFASs and BFRs.Missing: fracking | Show results with:fracking
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Critical Review on Bromate Formation during Ozonation and Control ...
Bromide Removal Electrochemical processes can remove ≤35% of bromide from natural waters in laboratory batch and continuous flow systems. During the process, ...
[136]
Linear and Non-Linear Modelling of Bromate Formation during ...
Apr 13, 2023 · The literature reports that bromate formation during the ozonation of water is influenced by bromide concentration and ozone dose as the ...
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Cytotoxicity Comparison between Drinking Water Treated by ...
Aug 28, 2023 · Brominated species are typically more cytotoxic and genotoxic than their chlorinated analogs. ... DBPs) are generally more cytotoxic and ...
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Evaluating regulatory scenarios to limit U.S. nationwide exposure to ...
Sep 4, 2023 · These studies generally find that brominated DBPs contribute higher toxicity than their chlorinated analogues, even when they form at lower ...
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Comparison of UV/chloramine disinfection of methylamine water in ...
This work illustrated HNMs formation from methylamine and the significant impacts of Br − on HNMs generation during UV/chloramine disinfection.
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Effects of bromide ion on the formation and toxicity alteration of ...
Aug 10, 2025 · Therefore, UV/chloramine combined disinfection may reduce the chloramine dosage, kill chlorine-resistant microorganisms, and ensure long-lasting ...
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Bromate removal during transition from new granular activated ...
Bromate removal by activated carbon after ozonation is a subject of concern, since bromate is commonly found in the ozonation of bromide-containing water.
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[PDF] Bromate formation control by enhanced ozonation: A critical review
Nov 30, 2020 · Although the EOPs are able to effectively remove emerging contaminants, several studies reported the formation of bromate, which has drawn ...
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Bromide in water | Metrohm
Bromide concentrations in seawater are generally between 65–80 mg/L, whereas ... The bromide concentration in fresh water is normally lower than 0.5 mg/L.
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Contaminant effects on the teleost fish thyroid - Wiley Online Library
Nov 5, 2009 · Methyl bromide is moderately toxic to fish with a 96-h LC50 of 10 to 15 mg/L [128, 129], but the bromide salts are much less toxic [130]. ...Overview Of The Thyroid... · Studies Of Thyroid... · Planar Halogenated Aromatic...<|separator|>
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National Primary Drinking Water Regulations | US EPA
The National Primary Drinking Water Regulations ( NPDWR) are legally enforceable primary standards and treatment techniques that apply to public water systems.
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Analysis of bromate in drinking water according to ISO 11206 and ...
EU and US EPA regulations set the maximum allowable bromate concentration in drinking water at 10 μg/L.<|separator|>
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Estimating European historical production, consumption and ...
▻ European atmospheric emissions of BDE-209 is predicted to peak in 2004 at 10 tonnes/year. ▻ The waste management phase is responsible for the majority ...
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[PDF] Bromine flame retardants – life-savers or eco villains? The ... - SCI
▫ Cost effective technology for flame retarding a wide range of different ... Flame retardants make ignition less likely and limit the rate of fire growth.
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[PDF] halogenated-flame-retardants-do-the-fire-safety-benefits-justify-the ...
Brominated and chlorinated chemicals are the least expensive way to meet flammability requirements. When the regulations leading to their use were implemented, ...