Abstract
Background
Chlorine-based disinfectants, such as bleach, are widely used in healthcare settings. However, their use has been linked to occupational respiratory risks. During disinfection, both chlorine gas and ultrafine particles (UFPs) can be generated, yet their exposure dynamics and health impacts remain poorly understood. This study aimed to characterize the emissions of chlorine gas and UFPs during disinfection under varying environmental and surface conditions to better understand exposure dynamics and inform risk mitigation strategies.
Methods
Controlled experiments were conducted in a sealed chamber to simulate typical healthcare disinfection scenarios. Bleach was tested under different conditions of temperature, light exposure, and in the presence of organic contaminants, including simulated vomit, urine, and blood. Chlorine gas was quantified using electrochemical sensors, while UFP emissions were measured using a condensation particle counter and mobility particle sizers. Additional validation experiments were performed in real-world office settings before and after cleaning.
Results
Chlorine gas was primarily emitted when bleach interacted with organic contaminants, particularly acidic substances such as simulated vomit, with an emission factor of 9.4 × 106 µg/min/m2. In contrast, UFP emissions were highest on clean surfaces under elevated temperature and light exposure, reaching up to 1.0 × 1011 particles/min/m2. Real-world validation confirmed that cleaning prior to disinfection significantly reduced chlorine gas emissions but led to increased UFP formation. Chlorine gas and UFP emissions were rarely observed simultaneously, indicating distinct and independent emission pathways.
Conclusions
Bleach-based disinfection generates airborne hazards through separate mechanisms: chlorine gas via reactions with organic residues and UFPs through secondary processes influenced by environmental conditions. These findings support enhanced cleaning protocols, improved ventilation, and the need for regulatory attention to UFP exposure in occupational settings.
Keywords: Chlorine, Disinfectants, Occupational health, Ultrafine particles, Respiratory conditions
Background
Occupational exposure to disinfectants in healthcare settings poses a significant public health concern, potentially affecting 65.1 million healthcare workers worldwide [1]. Among commonly used disinfectants, chlorine-based agents, such as sodium hypochlorite (bleach), are widely applied for surface disinfection due to their broad-spectrum antimicrobial activity and cost-effectiveness [2]. These agents are also recommended by major public health authorities, including the Centers for Disease Control and Prevention and the World Health Organization, in both routine healthcare settings and during outbreak responses [3, 4]. However, their use has been associated with an increased risk of respiratory conditions, including asthma, bronchial hyperresponsiveness (BHR)-related symptoms, and chronic obstructive pulmonary disease (COPD) [5]. Despite these concerns, the mechanisms underlying these health effects remain unclear, limiting the development of effective mitigation strategies. During disinfection procedures with sodium hypochlorite, both chlorine gas (Cl2) [6] and ultrafine particles (UFPs) can be generated [7], potentially contributing to occupational respiratory hazards. However, their individual and combined effects on respiratory health remain insufficiently characterized.
Cl2 exposure has been widely documented as a cause of acute respiratory distress, primarily due to its strong oxidative and mucosal-irritant properties. Upon inhalation, chlorine gas reacts with moisture in the respiratory tract to form hydrochloric acid (HCl) and hypochlorous acid (HOCl), which directly damage epithelial cells, increase airway permeability, and induce inflammation [8]. These reactions can lead to coughing, airway obstruction, and, in severe cases, reactive airway dysfunction syndrome [9]. The immediate irritant effects of chlorine gas make it a major driver of acute respiratory symptoms among healthcare workers and cleaning personnel.
Unlike Cl2, which induces direct chemical irritation, UFPs are small particles (< 100 nm in diameter) that penetrate deeper into the respiratory tract, reaching the alveolar region. These particles are formed when disinfectants, such as sodium hypochlorite, react with volatile organic compounds (VOCs) present in indoor environments [10]. Once deposited, they initiate oxidative stress at the cellular level, leading to the release of reactive oxygen species and the activation of inflammatory pathways [11]. The inflammatory response triggered by UFPs is more systemic and persistent, potentially contributing to chronic airway remodeling, fibrosis, and the progression of respiratory diseases such as asthma and COPD [12]. Additionally, UFPs have been shown to alter immune function, exacerbating susceptibility to respiratory infections and inflammatory lung diseases [13].
Although the acute effects of chlorine gas exposure are well documented, the chronic impact of UFP inhalation and its potential interactions with Cl2 exposure remain poorly understood. Current studies have largely relied on retrospective exposure assessments and self-reported symptoms, limiting the ability to determine primary contributors to occupational respiratory effects [14, 15]. To address this gap, this study systematically examines Cl2 and UFP emissions under various environmental conditions, providing a clearer understanding of occupational exposure risks associated with chlorine-based disinfection in healthcare settings.
Methods
An experimental study was designed to investigate the emission of chlorine gas and UFPs during chlorine-based disinfection, focusing on temperature, light exposure, and interactions between the disinfectant and various organic contaminants.
Tests were performed in a 1.80 m × 1.20 m × 2.20 m plexiglass chamber presenting a small opening for electrical cables and ducts. The air exchange rate of the chamber was measured by adopting a carbon dioxide decay method and resulted equal to 0.50 ± 0.03 h-1 [16]. To measure particle number concentrations in the sub-micrometric range, a butanol-based Condensation Particle Counter (CPC 3775, TSI Inc.) was used, capable of detecting particle sizes > 4 nm and measuring concentrations up to 1 × 107 particles cm-3. A Scanning Mobility Particle Sizer (SMPS) spectrometer, consisting of an Electrostatic Classifier (EC 3080, TSI Inc.) and a further CPC 3775, was used to measure particle size distribution in the sub-micrometric range. The setup included a sampling time of 135 s, an aerosol flow rate of 1.5 L min-1, and a sheath flow rate of 15 L min-1, measuring particle sizes from 6 to 220 nm. A Fast Mobility Particle Sizer (FMPS 3091, TSI Inc.) was also used, functioning as a stand-alone version of the SMPS with a sampling time of 1 s and measuring particle sizes from 5.6 to 560 nm. Inside the chamber, temperature and Cl2 concentrations were continuously measured using two certified GasBadge® Pro portable gas detectors (Cl2: range 0–100 ppm, sensitivity 0.1 ppm; temperature: range − 40 °C to 60 °C, ± 0.5 °C). Illuminance was measured with a lux meter sensor connected to a BABUC/m data acquisition system. Tests were conducted in a vessel made of white corrugated polypropylene sheets (1 m2) placed inside the chamber. Particle monitors were positioned outside the chamber, with inner air sampled through short tubes (15 cm) to minimize particle diffusion losses on the tube surfaces. Chlorine sensors, temperature sensors, and light irradiation sensors were positioned inside the chamber. Prior to each experiment, the vessel was cleaned with a soapy water solution and rinsed with water. A fan filter unit equipped with a High-Efficiency Particulate Air (HEPA) H14 filter and an F7 pre-filtration stage was operated at a flow rate of 850 m³ h-1 for 15 min to reduce the background particle concentration level. Each test was conducted on a different day to ensure complete air exchange and the restoration of ambient VOC concentrations inside the chamber. For each experiment, 500 mL of 0.5% sodium hypochlorite solution, aligned with Infection Prevention and Control (IPC) recommendations for surface disinfection in healthcare settings during outbreaks [17], was introduced into the chamber through an injection tube. The solution was prepared daily by diluting 50 mL of commercially available bleach (5% sodium hypochlorite, pH 13 ± 1) in 450 mL of water. Cl2 and particle measurements began before the injection of bleach to establish baseline levels. A control test was conducted under typical room light conditions (85 lux) and environmental temperature (26 °C), without the sodium hypochlorite solution, to confirm the absence of other chlorine gas and particle sources. Additional tests with bleach were conducted at low (22 °C), medium (26 °C), and high (38 °C) temperatures, as well as under radiation exposure of 1200 lux, simulating sunlight on a clear day using a Sanolux HRC 300 − 280 (Radium) lamp positioned 1 m above the vessel. To evaluate the impact of different organic contaminants on Cl2 and particle emissions during bleach-based disinfection, various substances were used, including vomit, urine, blood, and two different soaps. These substances were selected based on the assumption that they could commonly be encountered in healthcare settings as part of routine activities or accidental spills. Vomit was simulated using 10% HCl, a method previously employed to replicate the chemical properties of stomach contents [18]. Urine and blood were collected from a healthy adult male and a slaughterhouse-sourced chicken, respectively. For the soap solutions, a commercially available powder soap containing chlorine and a liquid soap containing ammonia were prepared according to the manufacturer’s specifications. The pH of the substances was measured using pH indicator strips (range 1–14, accuracy ± 1). All substances, in a volume of 15 mL, were placed inside the container, and bleach was subsequently injected. For each test, except those conducted in the office setting, three independent replicates were carried out. In the results section, the average emission factor values obtained from the three replicates were shown.
To validate the experimental results and to assess the influence of pre-cleaning activity, additional measurements of Cl2 and particle emissions were conducted during disinfection in two office environments. In Office 1, disinfection was performed without prior cleaning, where the floor had typical surface dust and light organic residues. In Office 2, a standard cleaning protocol was first carried out, which included mopping the floor with a detergent solution followed by rinsing with clean water and allowing the surface to dry before disinfection. The time to emission for both chlorine gas and particles was recorded from the injection of the sodium hypochlorite solution except for the real-setting validations due to a different injection procedure.
The emission factor (EF), i.e., the emission per unit time and unit cleaned surface, for both chlorine gas and UFPs, have been estimated using a well-known mass-balance equation derived by He et al. [19]:
 |
where 
and 
represent the peak and the initial concentration of the pollutant, 
is the average concentration, 
is the air exchange ratio, 
is the deposition rate, and 
is the time difference between initial and peak concentrations.
Results
The controlled experiments provided a comprehensive assessment of Cl2 and particle emissions under different environmental conditions and in the presence of organic contaminants commonly encountered in healthcare settings. The results are shown in Fig. 1, where a heatmap illustrates the variations in Cl2 and UFP emissions across test conditions. No Cl2 was detected under control conditions without bleach, supporting the conclusion that bleach was the source of chlorine emissions in subsequent experiments.
Fig. 1.
Chlorine gas and ultrafine particle emissions under varying conditions and organic contamination. The heatmap illustrates (A) chlorine gas (Cl2) and particle emissions across test conditions (Cl2 emissions are reported in µg/min/m², and particle emissions are reported in particles/min /m2) and (B) time to emission for both Cl2 and particles (seconds). Environmental conditions (C) include different temperatures (low, medium, and high), light radiation (1200 lux), and interactions with various organic substances (vomit, urine, blood, and soap with chlorine or ammonia). Real-world validation tests were conducted in two office settings before and after routine cleaning. < LOD, below the limit of detection
Effect of temperature on Cl2 and particle emissions
At low (22 °C) and medium (26 °C) temperatures, Cl2 emissions remained undetectable (in fact the concentration in the chamber was < 0.1 ppm), and the particle emission rate was relatively low (3.8 ± 0.04 × 109 and 3.5 ± 0.06 × 109 particles/min/m2, respectively). However, at high temperatures (38 °C), Cl2 emissions reached 1.5 ± 0.01 × 102 µg/min/m2, accompanied by the highest recorded particle production (6.6 ± 0.0074 × 1010 particles/min/m2). We highlight that particle emissions were entirely in the ultrafine range, as evidenced by the analysis of distributions measured using SMPS and FMPS (the same result was obtained for the tests discussed hereinafter, so it will not be repeated further). From the time to emission, it is possible to notice that the delay between bleach application and emission onset was significantly reduced at high temperatures, with UFPs detected within 64 s, compared to 971 and 1080 s at low and medium temperatures, respectively. During the high-temperature test, Cl2 emissions began 60 s after bleach injection.
Impact of radiation exposure
No detectable Cl2 concentration was observed when the experimental setup was exposed to light radiation of 1200 lux; however, UFP emissions were significantly elevated at 6.4 ± 0.0090 × 1010 particles/min/m2, comparable to high-temperature conditions, with a time to emission of 100 s.
Effect of organic contaminants on chlorine gas and particle emissions
The introduction of various organic contaminants significantly altered Cl2 and particle emissions. Contact with simulated vomit (pH 1–2) produced the highest recorded Cl2 emission rate (4.7 ± -0.12 × 103 µg/min/m2), with an emission onset time of 50 s. UFP emissions were measured at 4.1 ± 0.082 × 108 particles/min/m2, with onset occurring at 1000 s.
Urine (pH 5–6) produced a chlorine emission factor of 4.5 ± 0.069 × 103 µg/min/m2, with emission onset at 450 s. A UFP emission rate of 8.9 ± 0.036 × 109 particles/min/m2 was recorded, with onset at 493 s.
Contact with blood (pH 8–10) resulted in a chlorine emission factor of 7.5 ± 0.055 × 101 µg/min/m² with an onset time of 1480 s. UFP emissions were recorded at 1.8 ± 0.019 × 109 particles/min/m2, with an onset time of 720 s.
Soap with chlorine (pH 9–10) did not produce detectable Cl2 emissions but resulted in UFP emissions of 2.3 ± 0.93 × 109 particles/min/m2, with an onset time of 209 s. Interaction between bleach and soap with ammonia (pH 10–11) produced a chlorine emission factor of 2.3 ± 0.50 × 101 µg/min/m² with an onset time of 460 s. UFP emissions were recorded at 9.7 ± 1.2 × 109 particles/min/m2, with an onset time of 361 s.
Office setting
In Office 1 (prior to routine cleaning), Cl2 emission was recorded at 2.3 × 101 µg/min/m2 with an onset time of 580 s. UFP emissions were observed at 5.7 × 108 particles/min/m2 immediately after bleach application. In Office 2 (post-cleaning), no detectable Cl2 emission was recorded, but UFP emissions were observed immediately after bleach application at a rate of 3.2 × 109 particles/min/m2.
Discussion
This study systematically examined chlorine gas and ultrafine particle emissions under various environmental conditions to provide a clearer understanding of occupational exposure risks associated with chlorine-based disinfection. The findings identify two distinct exposure pathways: the release of gaseous chlorine through reactions between bleach and organic contaminants, and the formation of ultrafine particles driven by environmental factors such as temperature and light intensity. Each pathway presents unique health concerns, with chlorine gas posing an acute inhalation hazard [20] and UFPs contributing to long-term respiratory risks [21]. Figure 2 summarizes the main findings of this study, including health impacts, emission dynamics, and chemical reactions.
Fig. 2.
Mechanisms, health effects, and emission dynamics of chlorine gas and UFPs during disinfection. The figure illustrates the distinct pathways of chlorine gas and UFP emissions and their associated health effects. Chlorine gas exposure primarily leads to the formation of hydrochloric acid (HCl) and hypochlorous acid (HOCl) upon contact with moisture in the respiratory tract, causing direct chemical irritation, increased airway permeability, and inflammation. This can lead to acute respiratory symptoms such as bronchial irritation and reactive airway dysfunction syndrome. In contrast, UFP exposure induces oxidative stress and the release of reactive oxygen species, which damage cell membranes and trigger apoptosis, contributing to chronic airway remodeling, fibrosis, asthma, and chronic obstructive pulmonary disease (COPD). Systemic inflammation linked to UFP exposure increases the risk of cardiovascular diseases and exacerbates inflammatory lung diseases. The middle section highlights the environmental and chemical conditions influencing emissions. The lower section provides a schematic of sodium hypochlorite dissociation and the formation of chlorine gas, ultrafine particles, and toxic gases through reactions with acids, nitrogenous compounds, environmental factors, and volatile organic compounds (VOCs). In particular, temperature and radiation reduce the stability of bleach by promoting the formation of its less stable components (HOCl and Cl2), which subsequently undergo photochemical degradation, producing radical species such as Cl• and OH•. These radical species oxidize volatile organic compounds in the environment, leading to the formation of secondary organic aerosols (SOAs). The equilibrium between HOCl and ClO- is governed by pH; when pH decreases (acidification), more HOCl (which is less stable) is formed. Furthermore, HOCl and ClO- can react with HCl to form Cl2. Nitrogen-containing compounds can be oxidized by bleach, and the resulting products may undergo chlorination to form chloramines, which are toxic gases
We found that under conditions that can reasonably be assumed to reflect those commonly found in healthcare settings (22–26 °C temperature, typical light exposure, and clean surfaces), UFP emissions were detected within approximately 15 min without any chlorine gas release. Since the inflammatory response triggered by UFPs is more systemic and persistent, potentially contributing to chronic airway remodeling, fibrosis, and the progression of respiratory diseases, our findings may offer a hypothesis for the pattern reported in occupational health studies, where adverse effects associated with chlorine-based disinfection are more frequently linked to systemic inflammation and chronic diseases such as asthma and COPD than to acute respiratory symptoms. While further studies are needed, it is plausible that UFP exposure, rather than chlorine gas alone, plays a contributing role in the respiratory health issues observed in healthcare workers.
At high temperatures (38 °C), UFP emissions reached the highest value recorded in the study (6.6 × 1010 particles/min/m2), while Cl2 release was observed in minimal quantities. Notably, both emissions began in just one minute after bleach introduction. This suggests that elevated temperatures destabilize hypochlorous acid, increasing both chlorine volatilization and aerosol formation [22].
Similarly, exposure to visible light amplified UFP emissions to nearly the same level as observed at high temperatures, with emissions beginning within two minutes of bleach injection. However, no detectable Cl2 was produced, indicating that photochemical reactions promote aerosol formation without affecting chlorine stability [23].
These findings underscore the importance of considering ambient temperature and lighting conditions when evaluating exposure risks in healthcare and laboratory environments. Given that many tropical and warm-climate countries experience consistently high temperatures and intense sunlight, the risk of UFP exposure may be significantly higher in these settings, particularly in poorly ventilated healthcare facilities and enclosed workspaces where disinfectants are frequently used. Furthermore, the rapid onset of emissions under both high temperature and light conditions may further increase exposure risks, as workers are likely to remain in close proximity to the source when emissions occur.
The chlorine gas exposure pathway was most pronounced when bleach reacted with biological fluids. Simulated vomit resulted in the smallest recorded particle emission but produced the highest Cl2 emission within less than a minute. The rapid reaction and high emission underscore a severe inhalation hazard. This significant chlorine emission is likely due to acidic fluids, in this case, HCl, reacting with HOCl to produce Cl2 and water [24]. Similarly, urine, with a pH between 5 and 6, generated lower Cl2 emissions producing higher UFP emissions with onset occurring within less than 10 min after bleach introduction. These data suggest that nitrogenous compounds promote chlorine volatilization while simultaneously contributing to aerosol formation [2]. In contrast, contact with blood, with pH values between 8 and 10, triggered minor UFP emissions and minimal Cl2 release, with emission times ranging from 12 to 24 min. This suggests that the use of bleach on blood spills may represent a negligible risk of exposure. Powder cleaners with chlorine resulted in minimal UFP emissions and no detectable chlorine gas, while soap with ammonia led to higher UFP emissions and minimal Cl2 release. These findings underscore the potential risks associated with the co-use of bleach and ammonia-based cleaners.
Real-world validation experiments confirmed that pre-cleaning surfaces before disinfection significantly reduce chlorine gas emissions while promoting UFP emissions. In an uncleaned office, minimal Cl2 and UFP emissions were recorded. However, in a cleaned environment, Cl2 was undetectable, while UFP emissions were observed, supporting the hypothesis that the presence of certain organic contaminants drive chlorine gas formation, whereas secondary aerosol production is influenced by environmental conditions and VOC concentration [25], even on cleaned surfaces.
Unlike chlorine gas, which has well-defined occupational safety limits [26, 27], UFPs remain unregulated despite growing evidence linking them to serious health effects. The World Health Organization has classified UFPs as an emerging pollutant of concern [28], underscoring the urgent need for workplace monitoring and mitigation strategies.
While this study quantifies chlorine gas and UFP emissions under controlled conditions, factors such as humidity and surface characteristics may alter exposure dynamics. UFP composition was not analyzed, introducing uncertainties about toxicity. The study focused on individual contaminants, whereas mixed residues may influence emissions differently. Real-setting validation tests were not replicated, which limits the ability to assess variability in those scenarios. Personal exposure levels were not measured, highlighting the need for further occupational exposure assessments. To minimize occupational exposure risks, prevention strategies should target both chlorine gas and UFP exposure, particularly in healthcare facilities, laboratories, and sanitation services. Proper cleaning before disinfection can reduce chlorine gas emissions, while maintaining adequate ventilation is essential to limit the accumulation of both chlorine gas and UFPs in enclosed settings. Engineering controls such as localized exhaust systems and the use of alternative disinfectants like hydrogen peroxide and peracetic acid should be explored to reduce hazardous byproducts while maintaining antimicrobial efficacy. Future studies should assess ventilation strategies, including air exchange rates and filtration systems, to limit chlorine gas and UFP exposure in occupational settings. Real-world exposure assessments should monitor disinfectant byproducts in healthcare and laboratory environments. Further research is needed to characterize UFP toxicity, chemical composition, and long-term health effects.
Conclusions
This study provides a characterization of emission factors, which is essential for informing further research on exposure risk and absorbed doses, thereby guiding the development of future occupational safety limits. It highlights the occupational health risks of chlorine-based disinfection, demonstrating that chlorine gas and UFPs are generated through distinct mechanisms. Chlorine gas emissions were primarily linked to bleach interactions with organic contaminants, particularly acidic substances, while UFP formation was driven by temperatures and light exposure, even in clean environments.
These findings reinforce the need for stringent cleaning protocols, adequate ventilation, and worker protection measures to minimize exposure. While chlorine gas has established exposure limits, UFPs remain unregulated, despite evidence linking them to chronic respiratory and cardiovascular diseases. Addressing this regulatory gap requires further research to define exposure thresholds, assess long-term health effects, and develop workplace safety guidelines.
Given the risks associated with bleach-based disinfection, exploring safer alternatives could help reduce harmful airborne byproducts while maintaining microbial control. As chlorine disinfectants remain widely used, integrating air quality monitoring, engineering controls, and updated safety policies is essential to protect workers from both acute and chronic health risks.
Acknowledgements
Not applicable.
Authors’ contributions
LF, GB, LS and LF contributed to the formulation of overarching research goals and aims. LF, GB, LS, AC, and EC contributed to the design of the methodology. LF, AC, and LF ensured data curation and formal analysis. LF performed the preparation, creation, and writing of the initial draft. GB, LS, and LS reviewed and edited the initial draft. All authors reviewed the final manuscript.
Funding
This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
Data availability
All data generated or analysed during this study are included in this published article.
Declarations
Ethics approval and consent to participate
Not applicable.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
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Associated Data
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Data Availability Statement
All data generated or analysed during this study are included in this published article.