Scavenger-Probed Mechanisms in the Ultrasound/Chlorine Sono-Hybrid Advanced Oxidation Process

Abstract

Sonochlorination (US/chlorine) is an emerging sonohybrid advanced oxidation process whose performance reportedly surpasses that of its individual components. However, the underlying oxidant budget is still being debated. We mapped the mechanism by systematically probing the US/chlorine system with selective scavengers (ascorbic acid, nitrobenzene, tert-butanol, 2-propanol, and phenol), competing anions (nitrite), and natural organic matter (humic acid). The kinetic hierarchy US/chlorine > US > chlorine remained consistent across all conditions, though its magnitude depended heavily on the matrix composition. Efficient ^•OH traps, such as alcohols and nitrobenzene, only partially suppressed the US/chlorine system. However, they greatly slowed sonolysis. This reveals a substantial non-^•OH channel in the hybrid process. Ascorbic acid eliminated synergy by stoichiometrically removing free chlorine. Phenol quenched HOCl and chlorine-centered radicals. Nitrite imposed a dual penalty by scavenging ^•OH and consuming HOCl via the nitryl chloride (ClNO₂) pathway. Humic acid acted as a three-way sink for ^•OH, HOCl, and chlorine radicals. These patterns suggest that reactivity is co-controlled by Cl^•, Cl₂^•−, and ClO^•. The results obtained are mechanistically consistent with cavitation-assisted activation of HOCl/OCl⁻ at pH 5–6, where HOCl concentration is maximal. This yields a mixed oxidant suite in which Cl₂^•− is the dominant bulk oxidant, Cl^• provides fast interfacial initiation, and ClO^• offers selective support.

1. Introduction

Azo dyes are designed to persist in water. Allura Red AC (ARAC), a widely used sulfonated dye, has a chromophore that resists conventional treatment. Advanced oxidation processes (AOPs) target these chromophores with short-lived radicals. Coupling ultrasound with chlorine has emerged as an effective sono-hybrid AOP for ARAC, consistently outperforming sonolysis or chlorination alone. While this indicates genuine process synergy, it raises the question of which oxidants are responsible. Recent studies [1,2] on ARAC have shown that the combination of ultrasound and chlorine accelerates decolorization and mineralization beyond what would be expected from the sum of the individual processes. This motivates a mechanistic dissection of the oxidant budget that underpins this gain.

AOPs have been extensively studied for their ability to generate highly reactive species capable of degrading persistent pollutants. Recent studies have demonstrated the versatility of AOPs in various systems and matrices [3,4]. These results underscore the importance of exploring hybrid approaches, such as sonochlorination.

Ultrasound works through a process called acoustic cavitation. Bubbles form and grow before collapsing violently into transient hot spots that thermolyze water and solutes. This process produces ^•OH and H^• radicals, which create steep concentration and temperature gradients at the bubble–liquid interface [5,6]. The spatial localization of primary radicals and the frequency/gas dependence of cavitation determine the efficiency with which hydrophilic contaminants encounter oxidants released from interfacial zones in the bulk. These well-established sonochemical fundamentals explain why the oxidation of soluble dyes using only ultrasound is often limited by ^•OH radicals and dependent on interfacial transport.

Adding chlorine fundamentally changes this representation. In water, the speciation of chlorine (HOCl/OCl⁻; pKa ≈ 7.5–7.6) controls electrophilicity and activation pathways. Beyond direct chlorination, chlorine can be activated into reactive chlorine species (RCS), which complement ^•OH. These RCS include the chlorine atom (Cl^•), the dichloride radical anion (Cl₂^•−), and the chlorine monoxide (ClO^•). For more information on RCS generation and reactivity, see foundational kinetic compilations and recent AOP reviews [1,2,7,8,9,10,11,12,13]. A large body of kinetic data shows that these chlorine-centered radicals react selectively and often rapidly with electron-rich aromatics and azo nitrogens in patterns distinct from the indiscriminate behavior of ^•OH. Ultrasound provides a novel route to the same suite of RCS through HOCl/OCl⁻ cavitation-assisted reactions with H^•/^•OH in and around collapsing bubbles.

However, the dominant oxidant and its location in the sonoreactor during sonochlorination remain topics of debate. Cl^• is highly reactive yet short-lived, quickly converting to Cl₂^•− in chloride-containing water. Cl₂^•− is longer-lived and diffuses into the bulk, favoring outer-sphere electron transfer with electron-rich substrates. ClO^• exhibits distinct selectivity, reacting swiftly with activated moieties yet weakly with saturated alcohols. To understand these concurrent channels alongside the ever-present ^•OH, targeted probes and quantitative kinetics are required instead of relying on bulk performance alone.

In the present study, we address this gap using a scavenger-probed framework to analyze US/chlorine oxidant pathways. This framework uses a panel that includes ascorbic acid (AA), which is a fast and stoichiometric chlorine quencher, as well as nitrobenzene (NB) and the alcohols tert-butanol (TBA) and 2-propanol (IPA). These are classical, well-quantified ^•OH probes. The panel also includes phenol (Ph), which is an electron-rich competitor that is highly reactive toward Cl^•/Cl₂^•− and HOCl. The panel includes nitrite and humic acid (HA) as matrix components that impose dual (radical and chlorine) sinks. This approach expands the sonochlorination process beyond performance reports to include a radical-resolved mechanism by leveraging well-vetted kinetic frameworks for chlorine radicals and classical ^•OH chemistry.

2. Results and Discussion

2.1. ARAC Degradation by Chlorination, US and US/Chlorine

Figure 1 illustrates the changes in ARAC concentration (C/C₀) over time for three treatments: chlorination alone, ultrasonication alone, and a combined ultrasound/chlorine process. Two patterns immediately emerge. First, chlorination alone is the slowest method of decolorization/mineralization, as evidenced by the curve’s gradual decay. Second, ultrasonication alone rapidly removes the dye in the early stages, reflecting the fast kinetics of the generated hydroxyl radicals toward the azo nitrogens and the activated aromatic positions. Most importantly, sonochlorination degrades ARAC far more rapidly than either process alone, outperforming the sum of their individual rates and demonstrating genuine synergy. Hamdaoui et al. [1] quantified this effect, finding synergy indices between ~1.7 and 2.2 (and even higher under some metrics). Another paper [2] from the same research group showed a 320% rate enhancement relative to the additive expectation at pH 5.5.

Ultrasonic cavitation produces ^•OH and H^• radicals within collapsing bubbles and their surroundings. In the presence of HOCl/OCl⁻, these species, along with the high local temperatures, convert chlorine into reactive chlorine species (RCS), such as Cl^•, ClO^•, and Cl₂^•−. These RCS operate alongside ^•OH. RCS are selective electrophiles that efficiently attack azo nitrogens and electron-rich aromatic moieties. Several RCS have longer lifespans, enabling them to diffuse away from the bubble interface into the bulk solution. This broadens access to hydrophilic sulfonated dyes, such as ARAC. The combined radical suite and improved mass transfer explain why the sonochlorination curve is steeper. Figure 1 also shows that US alone surpasses chlorination alone for ARAC. This is not paradoxical. ARAC is unusually sluggish toward HOCl in this pH range, where HOCl predominates. Thus, chlorination alone removes little dye within the same time frame. Meanwhile, sonolysis provides an interfacial flux of ^•OH, which can bleach and oxidize the chromophore. Fundamental sonochemistry supports this interpretation. Cavitation restricts primary radical generation to the interior of bubbles and the bubble–liquid interface. This results in steep spatial gradients in radical availability. For nonvolatile, hydrophilic solutes like ARAC, degradation depends on transporting reactive species from these interfacial zones to the bulk. Recent modeling and reviews [14] demonstrate that ^•OH penetration depths are limited and strongly frequency-dependent. These findings help explain the moderate slope of the US-alone curve and the substantial increase when RCS are produced concurrently and can diffuse farther.

Based on the observed kinetic hierarchy in Figure 1, i.e., US/chlorine > US > chlorine, the next step was to deconvolute the oxidant chemistry. To accomplish this, targeted scavenger/probe tests were designed around the species involved in sonochlorination.

2.2. Ascorbic Acid

Figure 2 shows ARAC destruction by (a) ultrasonication and (b) sonochlorination in the presence of AA (1 and 10 mM). As shown in the two panels, the addition of AA, a rapid two-electron reductant and well-known chlorine quencher, consistently prevents the removal of ARAC during ultrasonication and sonochlorination. This inhibition is far more pronounced when chlorine is present. In drinking water treatment, AA reacts with chlorine (HOCl/OCl⁻) to form chloride with essentially instantaneous kinetics (within seconds) and a 1:1 stoichiometric ratio [15]. This reaction produces dehydroascorbic acid. This explains why AA is a standard quenching agent for chlorine/disinfection by-products sampling and why even mM concentrations of AA can extinguish oxidant activity at sub-mM chlorine doses. In sonochlorination system, 1 mM AA is four times a 250 µM chlorine dose, and 10 mM is forty times. Thus, the nearly flat traces at 10 mM AA in the sonochlorination panel are consistent with immediate dechlorination, which prevents sonochlorination altogether.

In the ultrasonication-only panel, the monotonic slowdown of ARAC decay with increasing AA concentration reflects AA’s role as a bulk-phase radical scavenger. Cavitation generates ^•OH radicals at or near collapsing bubbles. Since ARAC is hydrophilic, it primarily reacts with diffusing ^•OH. AA reacts with ^•OH at the diffusion limit (k ≈ 10¹⁰ M⁻¹ s⁻¹) by intercepting radicals before they reach dye molecules. AA can also reduce secondary oxidants, such as H₂O₂, thereby lowering the net oxidative flux. The result is a shallower decay despite the continuous production of radicals by ultrasound. This qualitative trend aligns with sonochemical fundamentals and scavenger tests that attribute a significant portion of dye destruction to ^•OH radicals.

In the sonochlorination panel, AA is more effective than US alone at suppressing dye degradation for two reasons. First, AA removes the chlorine before it can be activated by ultrasound. In other words, it eliminates HOCl/OCl⁻ before they can convert into RCS, such as Cl^•, Cl₂^•−, and ClO^•. These RCS are responsible for the synergy of the US/chlorine process for ARAC. This explains why the 10 mM AA curve scarcely decays; the enabling oxidant is quenched stoichiometrically at the outset. Second, even when some chlorine survives, AA remains a rapid one-electron donor for RCS. Kinetic compilations demonstrate that strong reductants react with Cl₂^•− at 10⁷–10⁹ M⁻¹ s⁻¹, thereby dampening the RCS-driven pathways that typically cause the US/chlorine process to outperform the individual processes.

Figure 2a,b illustrate two design and diagnostic points. When interpreting sonochlorination kinetics, it is important to confirm the presence of residual chlorine. Otherwise, apparent process failures may be dechlorination artifacts. Using AA as a mechanistic probe yields valuable information. The significant difference in reactivity between ultrasonication alone and sonochlorination at the same AA levels indicates that the increased reactivity in US/chlorine comes from chlorine-derived RCS rather than ^•OH alone.

2.3. Nitrobenzene

Figure 3a shows that NB acts as a classic scavenger of sonochemically generated ^•OH radicals. Increasing the NB concentration from 0 to 0.1 to 1 mM progressively suppresses ARAC degradation under ultrasonication. Since NB reacts with ^•OH at near-diffusion-controlled rates (k = 10⁹ M⁻¹·s⁻¹), even sub-mM concentrations of NB can outcompete the dye for ^•OH in the bulk/interfacial region. This flattens the decay curve. Reported bimolecular rate constants for NB + ^•OH cluster around 1–3 × 10⁹ M⁻¹·s⁻¹ using multiple kinetic methods [16,17]. Furthermore, moderately hydrophobic aromatics such as NB accumulate at the bubble–liquid interface where radical fluxes are highest. Thus, NB is particularly effective at intercepting sonochemically produced ^•OH radicals before they reach ARAC. These features explain the strong inhibition observed at 1 mM NB (nearly time-invariant C/C₀) and the partial inhibition observed at 0.1 mM.

Figure 3b shows the rapid decay expected under sonochlorination in the absence of NB. This reflects the activation of chlorine by ultrasound into a broader range of oxidants, including RCS (Cl^•, Cl₂^•−, and ClO^•), as well as ^•OH. Although introducing NB slows the process by removing ^•OH, degradation clearly persists, especially at 0.1 mM NB since NB is a poor sink for chlorine radicals compared to ^•OH. Kinetic compendia and UV/chlorine mechanistic studies treat NB as an ^•OH-selective probe because NB reacts poorly with Cl^• and other RCS [18]. However, many electron-rich aromatics react rapidly with both ^•OH and chlorine radicals. Thus, in the hybrid system, the pathway mediated by RCS continues to remove ARAC even when ^•OH is quenched. While this intervention reduces the disparity between sonochlorination and ultrasound-only processes, it does not entirely bridge the mechanistic gap.

NB’s differential effect across ultrasonication and sonochlorination panels enhances oxidant apportionment. In the US-only panel, ARAC loss is governed by the steady-state ^•OH flux that diffuses from the bubble interface. NB reduces this flux directly by rapidly scavenging ^•OH and indirectly by disrupting radical chain propagation. This results in significant inhibition in the ultrasonication panel. In sonochlorination, part of the oxidant budget is orthogonal to NB’s selectivity. RCS originate from chlorine transformations in and around collapsing bubbles. They react efficiently with azo nitrogens and activated rings of dyes. However, their reactivity toward electron-poor NB is limited, which explains the residual removal even at 1 mM NB. This interpretation aligns with comprehensive measurements of chlorine-radical rate constants, which demonstrate that Cl₂^•− reacts fastest with electron-rich aromatics and much more slowly as ring electron density decreases (e.g., nitro substitution) [9,18].

In practice, NB scavenger tests provide rigorous internal control of the sonoreactor. First, significant inhibition during ultrasonication confirms that ^•OH radicals drive sonolytic ARAC oxidation. Second, partial inhibition during sonochlorination demonstrates that RCS significantly contributes to the hybrid process. Third, the continued fast decay at zero NB emphasizes the importance of maintaining a pH close to the HOCl/OCl⁻ crossover point in order to promote sonication activation. Together, these results imply that sonochlorination’s superiority stems from an oxidant mixture of ^•OH and RCS that NB cannot fully quench.

2.4. Tert-Butanol

Figure 4a shows that TBA strongly inhibits ultrasonication-driven ARAC removal in a concentration-dependent manner. This suggests an ^•OH-driven sonolytic pathway. TBA is the standard, selective ^•OH scavenger in aqueous kinetics. The benchmark compilation by Buxton et al. [19] gives k_•OH-TBA ≈ (6–7) × 10⁸ M⁻¹ s⁻¹. Reactions with H^•/e_aq⁻ are negligible; therefore, even sub-mM concentrations of TBA can efficiently intercept diffusing ^•OH that escapes cavitation bubbles and reaches the near-interface/bulk where hydrophilic dyes reside. Consistent with this chemistry, increasing the TBA concentration from 0 to 1 mM and then to 10 mM progressively flattens the decay curve. However, at higher mM levels, TBA can alter cavitation chemistry because it is volatile and undergoes pyrolysis within collapsing bubbles, forming CH₃^• and associated products. This reduces net oxidant yields, an effect that has been directly observed in product and yield studies of TBA sonolysis. Together, these fundamental behaviors explain the pronounced inhibition observed in the ultrasonication panel.

Figure 4b shows that TBA levels suppress, but do not eliminate, ARAC degradation during sonochlorination. This partial resilience reflects the mixed oxidant suite generated when ultrasound activates chlorine, creating RCS in addition to ^•OH. TBA efficiently removes the ^•OH contribution but is a comparatively poor sink for Cl₂^•− (k_TBA+Cl2•⁻ ≈ 2.6 × 10⁴ M⁻¹ s⁻¹ [20]) and only a moderate sink for ClO^• (k_TBA+ClO• ≈ 1.3 × 10⁷ M⁻¹ s⁻¹ [10]). Thus, even at TBA concentrations of 1–10 mM, RCS-mediated oxidation of ARAC persists, yielding the shallower, but still descending, curves in the sonochlorination panel. Although Cl^• reacts rapidly with TBA (typically 10⁸–10⁹ M⁻¹ s⁻¹ [18]), Cl^• is short-lived and largely partitions into Cl₂^•−/ClO^• under aqueous, chlorine-rich conditions. Therefore, quenching Cl^• alone cannot fully collapse the hybrid pathway. These kinetic contrasts (^•OH vs. RCS) quantitatively account for the different degrees of inhibition in ultrasonication versus sonochlorination.

Two additional points from Figure 4b support this interpretation. First, unlike reductants such as AA, which stoichiometrically dechlorinate HOCl and prevent activation, TBA does not significantly consume chlorine. Therefore, residual HOCl continues to undergo sonochemical activation into RCS despite ^•OH scavenging in the studied pH range (HOCl predominates around pH 5–6, with a pKa ≈ 7.5 [1]). This process results in measurable dye loss. Second, continued removal at high TBA levels confirms that the previously reported synergy for ARAC under sonochlorination derives from RCS chemistry rather than from ^•OH alone.

TBA scavenging cleanly separates the contributions of the oxidants. In ultrasonication alone, ARAC degradation is governed by near-interface/bulk ^•OH, so TBA largely halts decay. However, in sonochlorination, RCS provide an additional oxidative pathway that TBA cannot efficiently suppress. RCS provide an additional oxidative pathway in sonochlorination that TBA cannot efficiently suppress. This preserves removal even at 10 mM. For mechanistic tests, low-mM TBA is appropriate for apportioning ^•OH versus RCS without significantly disrupting cavitation. However, at very high alcohol loadings, bubble chemistry and radical yields may be distorted. In practice, operating at a pH where HOCl dominates and minimizing strong reductants in the matrix maximizes sonochlorination performance. The presence of TBA-like alcohols primarily reduces the ^•OH portion of the oxidant budget.

2.5. 2-Propanol

Figure 5a,b demonstrate that the presence of IPA significantly impedes the removal of ARAC under ultrasonication and sonochlorination conditions. The magnitude of inhibition increases with the dose of IPA. In US-only operation, this behavior indicates a predominantly ^•OH-driven pathway. Since IPA is a fast classic ^•OH scavenger (k_•OH+IPA ≈ (1–2) × 10⁹ M⁻¹ s⁻¹ [19]), even sub-mM concentrations of IPA can efficiently intercept ^•OH radicals diffusing from cavitation bubbles to the near-interface/bulk region where the hydrophilic ARAC reside. The resulting reduction in effective ^•OH flux yields the progressively flatter decay observed at 1 and 10 mM. IPA suppresses ultrasonication oxidation by two complementary routes. First, it quenches ^•OH in the liquid phase at near-diffusion-controlled rates. This diverts radicals into benign products (e.g., acetone via H-abstraction) and lowers the steady-state oxidant level around the bubble. Second, because IPA is volatile and surface-active, mM additions can alter bubble chemistry by enriching the bubble–liquid interfacial zone. This diminishes interfacial ^•OH generation and related sonochemical signals. Together, these phenomena explain the significant decrease in performance at 10 mM IPA during ultrasonication.

In sonochlorination (Figure 5b), the degradation curve without IPA exhibits the anticipated rapid decay upon exposure to ultrasound. This reflects the sonochemical activation of HOCl/OCl⁻ into reactive chlorine species (RCS), specifically Cl^• and Cl₂^•−. These species work with ^•OH to create the hybrid process. Although adding IPA slows the process, degradation persists at 1 mM because ^•OH is not the only oxidant. The RCS continue to attack ARAC even when much of the ^•OH budget is quenched. This selectivity stems from the fact that IPA reacts extremely quickly with ^•OH (typically 10⁸–10⁹ M⁻¹ s⁻¹ for hydrogen abstraction from organics) and moderately with Cl₂^•− (k_Cl2•⁻_+IPA ≈ 10³–10⁵ M⁻¹ s⁻¹ [18]). Thus, a significant portion of the RCS pathway survives mM IPA. At 10 mM, however, there is enough IPA to intercept both ^•OH and a significant amount of RCS. This results in the collapse of much of the synergy and produces the near-plateau observed.

Finally, two practical notes follow from Figure 5a,b. First, since alcohol scavengers can also alter cavitation, mechanistic tests should use the lowest IPA concentration that yields clear trends to avoid artifacts. Second, the stronger inhibition observed with IPA relative to TBA is expected based on kinetics. IPA’s higher reactivity toward ^•OH, as well as its significant reaction with chlorine radicals, makes it a more potent, broad-spectrum quencher, especially at an elevated dose.

2.6. Phenol

Figure 6a shows that the presence of Ph significantly reduces ARAC removal during ultrasonication, with this reduction increasing as the amount of Ph increases. This pattern suggests an ^•OH-driven sonolytic pathway. Ph is a diffusion-limited ^•OH scavenger with a rate constant of (6–8) × 10⁹ M⁻¹ s⁻¹ at room temperature [19]. Therefore, even sub-mM concentrations of Ph can effectively intercept radicals diffusing out of collapsing bubbles into the near-interface/bulk where hydrophilic dye molecules reside. The reaction proceeds via fast addition to the aromatic ring to form hydroxycyclohexadienyl adducts/phenoxyl radicals. This diverts the oxidant budget away from the dye, flattening the decay curve. In aqueous sonochemistry, the sonochemical context remains consistent. H^•/^•OH radicals are produced inside/near bubbles, and pollutant oxidation in the bulk is limited by the flux of these short-lived species; the same flux that is quenched by Ph. Figure 6b shows that adding Ph to the sonochlorination system causes an even more dramatic slowdown. Adding 0.1 mM Ph markedly increases decay time, while adding 1 mM Ph nearly stops decay completely. This outcome can be explained by the fact that Ph is an exceptionally fast sink for chlorine radicals generated by ultrasound (sonoactivation). Cl^• reacts with Ph at a rate of approximately 10¹⁰ M⁻¹ s⁻¹ (near the diffusion limit) [9]. Cl₂^•− also rapidly oxidizes Ph at a rate of 10⁷–10⁹ M⁻¹ s⁻¹ [9]. These kinetics allow Ph to outcompete ARAC for both ^•OH and RCS. This collapses the synergy that normally causes the combination of ultrasound and chlorine to outperform the individual processes.

The contrast between panels in Figure 6a,b is mechanistically instructive. Without Ph, the combination of ultrasound and chlorine produces a true synergistic effect for ARAC because HOCl/OCl⁻ converts into a mixed oxidant suite, i.e., Cl^•, Cl₂^•−, and ClO^•, under ultrasonic cavitation. This suite works alongside ^•OH. However, introducing Ph selectively erodes this advantage. In addition to quenching ^•OH, as seen in panel (a), Ph efficiently removes RCS. This results in a plateau at 1 mM. Thus, the Ph experiments confirm that the extra reactivity in the US/chlorine mixture primarily stems from RCS pathways highly susceptible to scavenging by electron-rich aromatics.

2.7. Nitrite

Figure 7a,b show that the presence of nitrite greatly reduces the rate at which ARAC decays during ultrasonication and sonochlorination. This inhibition increases with nitrite dosage. With ultrasonication alone, adding 1–10 mM of nitrite yields flatter C/C₀-t curves than the nitrite-free run. With sonochlorination, the same nitrite levels severely dampen the initially steep decolorization observed in its absence. This behavior is expected because nitrite undergoes fast, near-diffusion-controlled reactions with the key radicals that drive both processes. In sonochemistry, the primary oxidant is ^•OH. Nitrite is one of the strongest aqueous ^•OH scavengers, with reported rate constants of ~10⁹–10¹⁰ M⁻¹ s⁻¹ (^•OH + NO₂⁻ → ^•NO₂ + OH⁻) [19]. Therefore, even a small amount of NO₂⁻ quickly diverts ^•OH away from the dye, lowering the effective oxidizing capacity of the bubble–liquid interface. The product, ^•NO₂, is a much more selective, albeit slower, electrophile toward many aromatics than ^•OH. Thus, the flux of radicals shifts from rapid mineralization/fragmentation toward slower nitration or no reaction. This manifests as higher residual C/C₀ at fixed times. The stronger inhibition in sonochlorination reflects the presence of additional nitrite sinks besides ^•OH. First, nitrite reacts directly and rapidly with free chlorine. Kinetic studies demonstrate that HOCl oxidizes NO₂⁻ via a mechanism involving the reversible formation of nitryl chloride (ClNO₂), followed by hydrolysis and secondary reactions. The overall rate law predicts significant chlorine consumption at circumneutral pH. In practice, however, nitrite immediately demands chlorine, depleting the HOCl/OCl⁻ necessary for sonochlorination. This forms RCS, such as Cl^•/Cl₂^•−. Furthermore, nitrite can intercept RCS. Kinetic and mechanistic analyses indicate that Cl^• is converted to Cl₂^•− in chloride media, which are prevalent during chlorination processes. These chlorine radicals undergo fast electron transfer with many anions and organics. Competition by NO₂⁻ further diverts radical flux away from the dye. Direct chlorine quenching and radical scavenging together explain why sonochlorination curves are more sensitive to nitrite than US-only curves.

Therefore, the following mechanistic picture unifies panels shown in Figure 7. Ultrasonic cavitation produces ^•OH, while chlorination produces HOCl/OCl⁻. These can be sonochemically activated to Cl^•/Cl₂^•−. Nitrite competes at three levels: (i) consuming ^•OH almost as soon as it is formed to produce ^•NO₂, (ii) consuming free chlorine through the ClNO₂ pathway (ultimately generating nitrate and chloride), thereby reducing the pool of oxidants that can be activated by ultrasound, and (iii) reacting directly or indirectly with RCS and further throttling the oxidative chain. Since ^•NO₂ is less reactive toward many dye chromophores than ^•OH/Cl^•, the radical mixture becomes less destructive, as demonstrated by the time courses.

Finally, two contextual notes help interpret Figure 7a,b. First, sonochemical studies report that high-power ultrasound can generate small amounts of nitrite and nitrate from air-saturated water. Although this is minor under conditions typically used for dye abatement, it further emphasizes how sensitive radical processes are to nitrate chemistry. Second, the HOCl–NO₂⁻ reaction is pH-dependent and often accelerates as the pH decreases (where HOCl dominates). Thus, the extent of inhibition in Figure 7b would be expected to increase under more acidic operating conditions. These considerations are consistent with the sharper loss of reactivity under sonochlorination than under ultrasound alone once nitrite is present.

2.8. Humic Acid

In both panels of Figure 8, an increase in HA consistently decreases the rate at which ARAC disappears. A stronger inhibitory effect is observed in the sonochlorination system than in ultrasonication alone. Figure 8a shows that HA effectively scavenges cavitation-generated ^•OH radicals in the bulk phase. Competition kinetics measurements across standard natural organic matter (NOM) isolates yield second-order ^•OH scavenging rate constants of approximately 10⁸ M⁻¹ s⁻¹ [21,22]. Thus, an HA concentration as low as 10–15 mg/L can significantly intercept diffusing ^•OH radicals that would otherwise oxidize the hydrophilic, sulfonated dye in the near-interface/bulk region. The outcome is fatigue of sonolytic decay (higher C/C₀ at fixed times) as the HA concentration increases. The much steeper loss of activity in sonochlorination arises because HA competes on three fronts. First, HA exerts direct chlorine demand. Second, the electrophilic HOCl/OCl⁻ reacts with electron-rich moieties in NOM, thereby reducing the amount of available disinfectant that ultrasound can activate. Third, HA is a major sink for reactive chlorine species formed during ultrasonication, principally Cl^• and Cl₂^•−; k_NOM–Cl• is typically 10⁸–10⁹ M⁻¹ s⁻¹, and k_NOM–Cl2•⁻ is lower but still substantial [18,23]. These values confirm that NOM efficiently diverts RCS away from target organics. This selective scavenging eliminates a significant amount of the extra reactivity that makes the combination of ultrasound and chlorine more effective than ultrasound alone. Additionally, the ^•OH scavenging observed in ultrasonication alone continues in the hybrid system, further flattening the time course once HA is present. Together, these pathways explain why a modest dose of HA only gradually slows US-only tests yet produces much greater inhibition when chlorine is present.

2.9. Mechanistic Insights

The scavenger trends were interpreted in terms of three RCS activated by ultrasound: Cl^•, Cl₂^•−, and ClO^•. These species were summarized based on their distinct contributions to the ultrasound/chlorine process.

Cl^• is a highly reactive interfacial oxidant that is strongly quenched by phenolic and humic sinks. Under acoustic cavitation, HOCl/OCl⁻ is activated via hot-spot reactions with sonolytic H^•/^•OH (e.g., H^• + HOCl → products including Cl^•; ^•OH + HOCl/OCl⁻ → ClO^•/Cl^• pathways). Cl^• then rapidly associates with Cl⁻ to establish the Cl^•/Cl₂^•− equilibrium. Cl^• reacts at near diffusion-controlled rates with electron-rich aromatics. Therefore, even modest additions of Ph or NOM (e.g., humic acid) efficiently quench Cl^• and suppress dye decay. In contrast, NB, an electron-poor compound and a standard ^•OH probe, reacts weakly with Cl^•. Thus, NB only partly inhibits the hybrid process, which again matches the data. Together, these patterns indicate a significant early role for Cl^• in sonochlorination, particularly at or near bubble–liquid interfaces. The steady-state level of Cl^• is controlled by its rapid capture by phenolic/humic sinks and conversion to Cl₂^•− in bulk water.

Cl₂^•− is a longer-lived bulk oxidant that dominates in the presence of alcohol probes. It forms within microseconds from the combination of Cl^• and Cl⁻ and remains active long enough to diffuse into the bulk, where it oxidizes electron-rich substrates via outer-sphere electron transfer. Cl₂^•− reacts extremely quickly with phenols (10⁷–10⁹ M⁻¹ s⁻¹) and much more slowly with saturated alcohols, such as TBA (10³–10⁴ M⁻¹ s⁻¹) and IPA (10⁵ M⁻¹ s⁻¹). Consequently, adding TBA or IPA only partially suppresses sonochlorination because, although they efficiently scavenge ^•OH, they are mediocre sinks for Cl₂^•−. Ph and humic acid, however, produce pronounced inhibition. The limited impact of NB on the hybrid process is consistent with its poor reactivity toward Cl₂^•− compared to phenols. Together with literature rate constants, these probe-specific outcomes suggest that Cl₂^•− significantly contributes to ARAC decay in the liquid bulk during US/chlorine treatment.

ClO^•, a selective oxidant, is formed alongside Cl^•. It is efficiently intercepted by reductants, such as AA, but shows little affinity for aliphatic alcohols. Reactions of ^•OH with HOCl/OCl⁻ produce ClO^•, which exhibits markedly different kinetics than Cl^•/Cl₂^•−. ClO^• reacts rapidly with electron-rich motifs (10⁸–10⁹ M⁻¹ s⁻¹). However, it is relatively inert toward saturated alcohols and simple aromatics. This selectivity explains why TBA and IPA do not fully quench the hybrid process, even though they suppress ^•OH. The ClO^• pathway remains operative. Strong inhibition by AA is expected because it quantitatively reduces chlorine and rapidly consumes one-electron oxidants such as ClO^•. Thus, AA depresses all RCS fluxes and collapses the synergy. The observed sensitivity of sonochlorination to humic matter aligns with ClO^•’s preference for electron-rich moieties in NOM. Overall, ClO^• provides a selective oxidation channel that runs parallel to Cl^•/Cl₂^•− and helps sustain degradation when ^•OH is masked by alcohol probes.

Nitrite rapidly and strongly consumes HOCl (k ≈ 7 × 10³ M⁻¹ s⁻¹ at neutral pH), forming short-lived nitrosyl chloride intermediates and ultimately nitrate. By depleting the molecular chlorine pool that feeds radical generation, NO₂⁻ suppresses all RCS formation. Therefore, it dampens both US alone (via ^•OH scavenging) and US/chlorine (via HOCl loss and RCS interception). Thus, the strong experimental inhibition in the presence of nitrite is consistent with its dual role as a chlorine quencher and radical sink.

Across the full probe suite, a coherent picture emerges. First, Ph and HA are fast, electron-rich sinks that strongly suppress the hybrid process. This suggests significant roles for Cl^• and Cl₂^•− (and, to a lesser extent, ClO^•), which react quickly with these moieties. Second, TBA and IPA are excellent ^•OH scavengers but comparatively poor Cl₂^•−/ClO^• sinks. They only partially inhibit sonochlorination, revealing that chlorine-centered radicals drive a large fraction of dye removal in the bulk. Third, NB is a classic ^•OH probe with low reactivity toward chlorine radicals. It dramatically inhibits US alone but only partially inhibits US/chlorine. This confirms the shift from hydroxyl-dominated chemistry to RCS-dominated pathways in the hybrid system. Fourth, AA collapses synergy by rapidly quenching chlorine.

These results are consistent with the literature on RCS generation and ClO^• selectivity. Together, these mechanistic fingerprints suggest that Cl^• initiates rapid interfacial attacks and generates Cl₂^•− in solution. Cl₂^•− is responsible for a significant portion of the bulk-phase oxidation of ARAC. Meanwhile, ClO^• provides a selective supporting pathway that is resistant to alcohol probes but sensitive to reductants and electron-rich competitors.

3. Materials and Methods

Ultrapure water was used for all solution preparation and sampling. Sodium hypochlorite (∼16% available chlorine) and Allura Red AC (ARAC; CAS 25956-17-6; C₁₈H₁₄N₂Na₂O₈S₂; 496.42 g/mol) were obtained from Sigma-Aldrich (St. Louis, MO, USA). All scavengers (AA, NB, TBA, IPA, Ph, NO₂⁻, and HA) were purchased from Sigma-Aldrich at the highest purity available.

Stock solutions of chlorine (100 mM, pH 5) and ARAC (500 mg/L, pH 5.5) were prepared, stored at 4 °C in the dark, and used to set experimental conditions at pH 5.5 and 25 °C.

Chlorination alone was carried out in a 200 mL water-jacketed glass cell under magnetic stirring at 300 rpm.

Ultrasonication experiments were performed with 150 mL of solution in a cylindrical, water-jacketed glass reactor. Ultrasonication was delivered at 600 kHz using a piezoelectric disk (4 cm diameter) bonded to a stainless-steel plate (5 cm diameter) fixed to the reactor bottom. The electrical input power was 120 W. Liquid temperature was controlled at 25 °C via the jacket and monitored with an immersed thermocouple. Acoustic power dissipated in solution, determined calorimetrically, was 23 W, corresponding to an average acoustic intensity of 1.83 W/cm².

ARAC concentrations were quantified by UV–Vis spectrophotometry (Biochrom WPA Lightwave II) at λ_max = 504 nm.

First-order rate constants are often used to compare the kinetics of pollutant degradation. However, the presence of radical scavengers invalidates the simple pseudo-first-order assumption due to competition for reactive species. Therefore, presenting individual kinetic curves more accurately reflects the interactions between pollutants and scavengers.

4. Conclusions

The scavenger series demonstrates the superiority of the US/chlorine system. This is because cavitation activates chlorine, creating reactive chlorine species (RCS: Cl^•, Cl₂^•−, and ClO^•), which work with ^•OH. This hybrid pathway remains active when ^•OH is suppressed by alcohols or NB. However, the pathway collapses when chlorine is stoichiometrically removed by AA, or when HOCl/OCl⁻ and RCS are outcompeted by fast electrophile scavengers, such as Ph, nitrite, and NOM. AA nearly abolishes sonochlorination because it rapidly and stoichiometrically dechlorinates HOCl/OCl⁻. Therefore, the strong inhibition observed verifies that an available chlorine pool is a prerequisite for sonochlorination. NB and alcohols (e.g., TBA and IPA) flatten US-only curves because they react with ^•OH at diffusion-controlled rates. The canonical rate constants are ~10⁹ M⁻¹ s⁻¹ for IPA, ~6–8 × 10⁸ M⁻¹ s⁻¹ for TBA, and ~10⁹ M⁻¹ s⁻¹ for NB. This indicates an ^•OH-controlled sonolytic pathway. However, under US/chlorine conditions, these same scavengers only partially inhibit at mM levels because they react much more slowly with Cl₂^•− (typically 10³–10⁵ M⁻¹ s⁻¹ for simple alcohols). This leaves part of the chlorine radical budget unintercepted. An RCS channel continues to degrade the dye. Ph uniquely damages the hybrid process because it competes on all three oxidant fronts: fast electrophilic substitution with HOCl/OCl⁻, diffusion-limited reaction with Cl^•, and fast outer-sphere oxidation by Cl₂^•− (10⁷–10⁹ M⁻¹ s⁻¹ for electron-rich aromatics). The near-arrest of dye loss at mM levels of Ph emphasizes the importance of the RCS/HOCl pathways and highlights the risk of chlorinated phenolic byproducts under chlorine exposure. Nitrite has a dual effect: it is an exceptionally strong ^•OH scavenger (^•OH + NO₂⁻ → ^•NO₂), and it consumes chlorine through the ClNO₂ pathway (HOCl + NO₂⁻ ⇌ ClNO₂ + OH⁻, followed by hydrolysis/NO₂⁻ attack). This depletes the oxidant that ultrasound would otherwise activate. The pronounced slowdowns measured in both US and US/chlorine systems result directly from established nitrite kinetics with ^•OH and HOCl. HA, a NOM surrogate, inhibits sonochlorination more than sonolysis because it simultaneously scavenges ^•OH. Humic acid (a NOM surrogate) depresses sonochlorination more than sonolysis because it simultaneously scavenges ^•OH (k_OH-NOM on the order of 10⁸ M⁻¹ s⁻¹ for typical isolates), imposes a chlorine demand via rapid reactions of HOCl/OCl⁻ with aromatic/activated moieties, and quenches chlorine radicals (k_NOM–Cl• ≈ 10⁸–10⁹ and k _NOM–Cl2•⁻ lower but still substantial), all of which shrink the oxidant budget that drives synergy.

The findings are mechanistically aligned with the ultrasonication-facilitated activation of HOCl/OCl⁻ within the pH range of 5–6, wherein HOCl predominates. This process creates an oxidant system consisting of Cl₂^•−, the primary oxidant in the bulk phase; Cl^•, a rapid initiator at interfaces; and ClO^•, a supportive, selective species. These findings provide the mechanistic basis for the process advantages reported in this study.

From a scaling-up perspective, cavitation activity and sonochemical reactions are strongly localized near the emitting surface or standing-wave antinodes. These reactions rapidly attenuate with distance due to wave damping and bubble shielding. Thus, strategies such as multipoint emitter arrays, focusing, flow-through cells, and/or enhanced mixing are usually necessary for treating large volumes of water and distributing active zones.