Why Hypochlorous Acid Is Not Safe for Daily Use on Skin Nor Your Eczema

Hypochlorous acid (HOCl) is everywhere in skincare right now. Brands are positioning it as a gentle, microbiome-friendly daily spray — safe for sensitive skin, safe for eczema, safe for everyone. The marketing is compelling.

But I can’t believe that more people aren’t talking more about this (!!)…

The science tells a different story.

What I want to share with you, is a citation-backed look at what peer-reviewed research actually says about HOCl: what it is, how it kills, what the selectivity claims are actually based on, and why daily application — even on healthy skin — raises legitimate concerns that no major HOCl brand is discussing.

And I’m not cherry-picking publications here that fit my concerns – I surveyed the entire literature, looking at the data.

I want you to know the dangers of what you are getting into, so that you can make the informed decision yourself.

A note to clinicians: The microbiome science covered in this post sits at the intersection of microbial ecology, evolutionary biology, and skin immunology — disciplines that sit outside most dermatology training curricula. This is not a criticism; it reflects how young the field is. The Human Microbiome Project only launched in 2007, and our understanding of skin microbial community dynamics is still rapidly evolving.

 My hope is that this post serves as a useful resource — a synthesis of the peer-reviewed literature on HOCl's mechanistic effects on the skin microbiome that may not have crossed your desk yet. The citations are all primary literature and freely accessible.

A note to everyone else: If your dermatologist has recommended HOCl for daily use, they are not wrong to trust an FDA-cleared ingredient with a good short-term safety profile. What this post adds is the microbiome layer — a dimension of skin health that is genuinely underrepresented in clinical training right now.

My goal is to give you more information, not to undermine your relationship with your doctor.

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HOCl is a weak acid and potent oxidant produced endogenously by neutrophils during the oxidative burst — the immune system's rapid-response mechanism for killing pathogens. The enzyme myeloperoxidase catalyzes its production from hydrogen peroxide and chloride ions inside the phagosome, a sealed intracellular compartment designed specifically to contain the reaction.¹

The fact that your immune system produces HOCl is frequently cited in marketing as evidence of its safety for daily topical use. This argument misunderstands the biology. When neutrophils generate HOCl, they do so:

Inside a sealed phagosome — a compartment that contains the reaction and protects surrounding tissue

In a transient burst lasting seconds — not sustained daily exposure across the entire skin surface

Aimed directly at a specific engulfed pathogen — not broadcast across the full microbiome

Spraying HOCl across your face twice daily is physiologically nothing like the oxidative burst. The context of production is entirely different.

 

"HOCl is an endogenous molecule" is a true statement. Using it to imply daily topical safety is a logical non-sequitur.

 

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HOCl kills through multiple simultaneous oxidative pathways. This is critical to understanding why selectivity claims are chemically implausible.

Peer-reviewed mechanism data^2,3,14,21 describes the following simultaneous attack pathways:

• Protein oxidation: HOCl oxidizes sulfhydryl groups on cysteine and methionine residues, causing irreversible protein unfolding and aggregation. This is considered a primary bactericidal mechanism. Davies (2016) ²¹ further details how this leads to protein peroxidation, where damaged proteins can actually perpetuate oxidative stress by reacting with neighboring molecules. These are considered primary bactericidal mechanisms.
• Amino acid halogenation: Chlorination of amino acid side chains (tyrosine, tryptophan, lysine) disrupts protein structure and function across the bacterial proteome.
• DNA damage: HOCl oxidizes DNA bases, causes strand breaks, and inhibits both replication and repair.
• ATP production collapse: Disruption of respiratory chain components and ATPase activity eliminates the bacterium's energy supply.
• Membrane disruption: HOCl degrades membrane lipids and inactivates membrane transport proteins, causing loss of cellular integrity.
• Nutrient uptake inhibition: Damage to transport proteins blocks the bacterium from absorbing nutrients.
• Protein aggregation induction: HOCl is a potent inducer of protein aggregation — a mechanism so severe that bacteria have evolved specific chaperone proteins (Hsp33, RidA, CnoX) as a defense response.

There is no targeting system in any of these mechanisms. HOCl reacts with organic matter — sulfhydryl groups, amines, lipids, nucleic acids — regardless of whether that organic matter belongs to a pathogen or a commensal organism. The chemistry is indiscriminate by definition.

 

HOCl doesn't pick sides. It destroys proteins, scrambles DNA, and shuts down energy supply — simultaneously, in every cell it contacts at sufficient concentration.

 

 

The Marketing Claim

Multiple HOCl brands claim that their products selectively target pathogenic bacteria while leaving beneficial commensal bacteria unharmed. This is the central claim used to justify daily use as "microbiome-friendly."

It is not supported by the peer-reviewed evidence.

The Most-Cited Study

The study most frequently cited in support of HOCl selectivity is a 2017 paper by Stroman et al., published in Clinical Ophthalmology, funded by NovaBay Pharmaceuticals (manufacturer of the HOCl product being tested).⁴ The study examined bacterial load reduction on periocular skin 20 minutes after application of 0.01% HOCl.

What the study actually found:

• S. epidermidis comprised 60% of all staphylococcal strains recovered from skin before treatment
• After HOCl application, bactericidal activity (≥99.9% reduction) was observed for ALL species tested
• S. epidermidis was killed at 99.9% reduction with  p<0.001 — a highly statistically significant result
• The difference between species was time-to-kill, not survival. Every species tested was dead at the endpoint.

The authors' conclusion that this finding "may be beneficial" because S. epidermidis was slightly slower to kill than S. capitis is speculative editorializing, not a data-supported selectivity claim. A difference in rate of killing is not selectivity. A 99.9% reduction in a commensal organism with p<0.001 is not sparing that organism. I also note here that organisms were tested in culture.

Head-to-Head Comparison Data

A broader time-kill study comparing HOCl against standard antiseptics found that HOCl at 0.01% exhibited bactericidal effects against both methicillin-resistant and methicillin-susceptible S. aureus and S. epidermidis, as well as S. capitis, S. pyogenes, P. aeruginosa, C. acnes, C. albicans, and S. xylosus.⁵ No differential susceptibility between S. aureus (pathogen) and S. epidermidis (commensal) was noted.

The selectivity narrative is not supported by the head-to-head data. When S. aureus and S. epidermidis are tested together, they are killed comparably. The "natural and selective" framing is marketing, not mechanism.

 

 

Atopic dermatitis (eczema) is characterized by skin microbiome dysbiosis — a disruption of the normal microbial ecosystem. Understanding what this means is essential to understanding why daily HOCl use is particularly problematic for this skin type.

The Dysbiosis Landscape in AD

Peer-reviewed characterization of the AD microbiome⁶ shows that eczema skin has:

• Reduced overall microbial diversity — lowest at actively affected sites
• Overgrowth of S. aureus in lesional skin — the primary driver of flares
• Depleted commensal staphylococci, including S. epidermidis — the organisms that normally provide protection

What S. epidermidis Actually Does

S. epidermidis is not a passive bystander. It is an active protector of skin health:

• It selectively kills S. aureus through bacteriocin production — a property demonstrated in both planktonic and biofilm conditions.⁷
• A lipopeptide from S. epidermidis enhances production of antimicrobial peptides in human keratinocytes and mouse skin, strengthening the innate immune response.⁶
• S. epidermidis colonization activates CD8+ skin-resident T cells via IL-1 signaling, limiting pathogen invasion.⁶
• In germ-free mouse models, mono-colonization with S. epidermidis was more protective against pathogen infection than germ-free skin — demonstrating its direct defensive function.⁶

The implication for HOCl use: eczema skin is already depleted of S. epidermidis. Daily application of an agent that kills S. epidermidis at 99.9% further depletes the very organism that is working to control S. aureus overgrowth — the primary pathogen driving eczema flares.

 

Drs. Nakatsuiji and Gallo in their Annals of Allergy, Asthma and Immunology article put it plainly: "Highly potent antimicrobials may result in a short-term improvement, but they can subsequently increase long-term" dysbiosis.⁶ This is precisely the concern with daily HOCl use on eczema skin.   

 

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The concerns do not apply only to eczema. Daily HOCl use on healthy skin raises three distinct evidence-based problems that are absent from virtually all consumer-facing HOCl content.

Problem 1: Disruption of a Functioning Ecosystem

A healthy skin microbiome is actively maintaining your skin. In Snell, Jandova and Wondrak (Frontiers in Oncology 2022)  explicitly lists "alteration of the commensal microbiome" as an expected outcome of inappropriate topical HOCl use⁸ — where "inappropriate" refers to daily cosmetic application, not wound care. Prescott et al. (2017) confirm that reduced microbial diversity is linked to the development of inflammatory skin diseases including atopic dermatitis, with evidence that microbiome disruption can predate disease development — not merely accompany it.^{9, 13}

Problem 2: Sublethal Exposure Selects for Resistance

This is the concern that receives almost no attention in the HOCl skincare space. When HOCl is applied topically, the concentration reaching bacteria in deeper skin layers is variable and almost certainly sublethal in many cases. The peer-reviewed data on what sublethal HOCl does is alarming:

• Sublethal HOCl concentrations induce antibiotic resistance through overexpression of efflux pumps and antibiotic resistance genes.³ Prior exposure to sublethal NaOCl increased bacterial resistance to multiple antibiotics by 1.4–5.6 fold. ³
• da Cruz Nizer et al. (2020) further details how bacteria utilize these global stress responses to survive reactive chlorine, emphasizing that sublethal exposure can lead to a "viable but non-culturable" (VBNC) state where bacteria remain present and potentially dangerous but are harder to detect.
• A 2024 study (Nam & Yoo) specifically identified the RND-type (Resistance-Nodulation-Division) efflux pump system as a key driver of this resistance following sublethal sodium hypochlorite (NaOCl) exposure. ¹⁹
• Sublethal HOCl triggers biofilm formation — a protective response in which bacteria aggregate in a matrix that makes them 100–1,000 times more resistant to antimicrobials than planktonic cells.^,20
• HOCl-specific gene expression triggers bacteria to switch from planktonic to biofilm lifestyle, increasing surface hydrophobicity and extracellular matrix production.¹⁰

In other words: daily HOCl use does not just fail to help — it may actively select for a harder-to-treat bacterial landscape on your skin.

Problem 3: No Long-Term Human Safety Data Exists

Despite the confident daily-use claims made by HOCl brands, there are no published longitudinal studies tracking the impact of repeated daily topical HOCl on the healthy skin microbiome. The only study attempting to measure real-world microbiome impact under sustained HOCl use is a 2025 preprint (meaning the paper hasn’t finished or gone through peer-review) from a Norwegian military field exercise¹¹, which explicitly stated: "the influence of stabilized HOCl on the skin microbiome under real-world conditions is unknown."

This is not a solved question. The daily-use safety story is extrapolated from wound care tolerance data — a completely different clinical context.

 

The absence of evidence of harm is not evidence of absence of harm — particularly when the known mechanism (indiscriminate oxidative killing) gives a clear biological reason for concern.

 

 

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Even setting aside the mechanistic concerns, there is a significant product integrity problem with the HOCl skincare category. HOCl is an unstable molecule that degrades rapidly with light, heat, and contact with organic matter.

A 2020 investigation of HOCl products sold online found that 30% had no label information on concentration and 50% had no information on pH or expiration date.¹²

HOCl efficacy is highly concentration- and pH-dependent.

 

You often cannot know what you are actually applying.

 

 

To be clear: HOCl has a well-validated role in specific contexts. The peer-reviewed evidence supports:

• Wound care and debridement — FDA-cleared, decades of clinical data, appropriate application
• Flare management in atopic dermatitis — modest clinical signal from small trials; risk/benefit may be acceptable in the acute infection setting. We haven’t released our paper yet on ceramides and the microbiome, but my concern here is that it may not be a good approach in flares, given the contribution of the microbiome to skin barrier and health.
• Post-procedure skin care — laser, surgery, where bacterial load reduction is the short-term goal
• Periocular hygiene — the context in which the most clinical data exists

The key distinction is context. Short-term, targeted, clinically-indicated use is very different from daily preventive application across an entire skin surface.

 

The key distinction is context. Short-term, targeted, clinically-indicated use is very different from daily preventive application across an entire skin surface.

 

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The HOCl skincare story is built on three pillars that do not hold up to scrutiny:

1. "Your body makes it, so it's safe": True that your body makes it. False that this makes daily topical use safe — the biological context is entirely different. I’d also argue that snake venom is “natural” – but you wouldn’t want to inject it at large doses!
2. "It selectively targets bad bacteria": Not supported by head-to-head data. Both S. aureus and S. epidermidis are statistically significantly killed at comparable rates and concentrations.
3. "Safe for daily use on sensitive/eczema skin": ZERO long-term microbiome data. I’m also concerned that the chemical mechanism of action is SO non-selective that it can  deplete the exact organisms’ eczema skin needs most. A documented risk of selecting for more resistant bacteria under sublethal (meaning lower) exposure.
   

 

Skin with eczema or sensitivity is already in a depleted, dysbiotic state. (You’ll see more evidence of this in our forthcoming peer-reviewed manuscript!) It needs its microbiome supported and rebuilt — not subjected to a daily broad-spectrum oxidative assault.

 

If this changed how you think about HOCl, pass it on. All we ask is a link back so the science stays attached to the source.

 

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[1] Ulfig A, Leichert LI. (2021). The effects of neutrophil-generated hypochlorous acid and other hypohalous acids on host and pathogens. Cellular and Molecular Life Sciences, 78(2), 385–414. https://pubmed.ncbi.nlm.nih.gov/32661559/

[2] Goemans CV, Collet JF. (2019). Stress-induced chaperones: a first line of defense against the powerful oxidant hypochlorous acid. F1000Research, 8:1678. https://pubmed.ncbi.nlm.nih.gov/31583082/

[3] Cortesão M et al. (2020). Surviving reactive chlorine stress: responses of Gram-negative bacteria to hypochlorous acid. Microorganisms, 8(8), 1220. https://pmc.ncbi.nlm.nih.gov/articles/PMC7464077/

[4] Stroman DW, Mintun K, Epstein AB, Brimer CM, Patel CR, Branch JD, Najafi-Tagol K. (2017). Reduction in bacterial load using hypochlorous acid hygiene solution on ocular skin. Clinical Ophthalmology, 11, 707–714. Funded by NovaBay Pharmaceuticals; three authors are NovaBay employees. https://pubmed.ncbi.nlm.nih.gov/28458509/

[5] Anagnostopoulos AG et al. (2018). 0.01% Hypochlorous acid as an alternative skin antiseptic: an in vitro comparison. Dermatologic Surgery, 44(12), 1489–1493.

[6] Nakatsuji T, Gallo RL. (2019). The role of the skin microbiome in atopic dermatitis. Annals of Allergy, Asthma & Immunology, 122(3), 263–269. https://www.annallergy.org/article/S1081-1206(18)31503-5/fulltext

[7] Jang H et al. (2024). Skin microbiota: pathogenic roles and implications in atopic dermatitis. Frontiers in Cellular and Infection Microbiology. https://www.frontiersin.org/journals/cellular-and-infection-microbiology/articles/10.3389/fcimb.2024.1518811/full

[8] Snell JA, Jandova J, Wondrak GT. (2022). Hypochlorous acid: from innate immune factor and environmental toxicant to chemopreventive agent targeting solar UV-induced skin cancer. Frontiers in Oncology, 12, 887220. https://www.frontiersin.org/journals/oncology/articles/10.3389/fonc.2022.887220/full

[9] Prescott SL et al. (2017). The skin microbiome: impact of modern environments on skin ecology, barrier integrity, and systemic immune programming. World Allergy Organization Journal, 10(1):29. doi: 10.1186/s40413-017-0160-5

[10] Conner JG et al. (2019). Bacterial defense systems against the neutrophilic oxidant hypochlorous acid. Infection and Immunity, 88(1). https://journals.asm.org/doi/10.1128/iai.00964-19

[11] Bakkemo KR et al. (2025). Longitudinal analysis of the hand microbiome in response to chlorine-based antiseptic use during a military field exercise. bioRxiv (preprint, not yet peer-reviewed). https://www.biorxiv.org/content/10.1101/2025.11.20.689467.full.pdf

[12] Ishihara K et al. (2020). Inappropriate sales of hypochlorous acid solution in Japan: an online investigation. JMIR Public Health and Surveillance, 6(4). https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7573454/

[13] Fyhrquist N, Muirhead G, Prast-Nielsen S et al. (2019). Microbe-host interplay in atopic dermatitis and psoriasis. Nature Communications, 10(1):4703. doi: 10.1038/s41467-019-12253-y. PMID: 31619666

[14] Natarelli N et al. (2023).. Hypochlorous acid: Applications in dermatology. Journal of Integrative Dermatology. doi: 10.64550/joid.1d4y5r09 — https://jintegrativederm.org/doi/10.64550/joid.1d4y5r09

[15] Draelos Z, Cash K. (2012).. Evaluation of a gel formulation of hypochlorous acid and sodium hypochlorite to reduce pruritus in mild to moderate atopic dermatitis. Poster, Winter Clinical Dermatology Conference, Maui, January 2012 [Conference poster — not peer-reviewed. Funded by Onset Dermatologics.] — https://www.globenewswire.com/news-release/2012/02/28/1158732/0/en/Onset-Dermatologics-Launches-Aurstat-R-Kit.html

[16] Berman B, Nestor M. (2017).. Investigator-blinded, randomized study evaluation of HOCl in the treatment of atopic dermatitis-associated pruritus. SKIN: The Journal of Cutaneous Medicine. 1(supp), 40. doi: 10.25251/skin.1.supp.39 [Conference supplement — not standard peer review. Funded by Exeltis.] — https://mauiderm.com/an-investigator-blinded-randomized-study-evaluating-hypochlorous-acid-hocl-in-the-treatment-of-atopic-dermatitis-associated-pruritus/

[17] Fukuyama T, Ehling S, Cook E, Bäumer W. (2017).. Hypochlorous acid is antipruritic and anti-inflammatory in a mouse model of atopic dermatitis. Clinical & Experimental Allergy. 48(1), 78–88. doi: 10.1111/cea.13045 [Mouse study — NC/Nga mice.] — https://onlinelibrary.wiley.com/doi/full/10.1111/cea.13045

[18] Fukuyama T, Ehling S, Wilzopolski J, Bäumer W. (2018).. Comparison of topical tofacitinib and 0.1% hypochlorous acid in a murine atopic dermatitis model. BMC Pharmacology and Toxicology. 19:37. doi: 10.1186/s40360-018-0232-3 — https://pubmed.ncbi.nlm.nih.gov/29970189/

[19] Nam J-H, Yoo JS. Sublethal Sodium Hypochlorite Exposure: Impact on Resistance-Nodulation-Cell Division Efflux Pump Overexpression and Cross-Resistance to Imipenem. Antibiotics. 2024; 13(9):828. https://doi.org/10.3390/antibiotics13090828

[20] Romanowski EG, Stella NA, Yates KA, Brothers KM, Kowalski RP, Shanks RMQ. In Vitro Evaluation of a Hypochlorous Acid Hygiene Solution on Established Biofilms. Eye Contact Lens. 2018 Nov;44:S187-S191. doi: 10.1097/ICL.0000000000000456. PMID: 29369234

[21] Davies MJ. Protein oxidation and peroxidation. Biochem J. 2016 Apr 1;473(7):805-25. doi: 10.1042/BJ20151227. PMID: 27026395

[22] da Cruz Nizer WS, Inkovskiy V, Overhage J. Surviving Reactive Chlorine Stress: Responses of Gram-Negative Bacteria to Hypochlorous Acid. Microorganisms. 2020; 8(8):1220. https://doi.org/10.3390/microorganisms8081220

 

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