January 2008 Issue

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Chemically-induced Rashes

Roy Vore, Ph.D.

Rashes are a common complaint with both pool and spa users. Rashes may be caused by a reaction to chemicals in the water or by a bacterial infection (see “Recreational Water Illnesses (RWI’s) in Spas” in the September 2007 RWQ newsletter, http://www.apsp.org/159/index.aspx). This article will focus on chemically-induced rashes.

The first step in investigating rash outbreaks should be to identify the cause. The simplest way to differentiate chemically- and bacterially-induced rashes is the incubation period. Nearly all chemically-induced rashes develop clinical symptoms within 24 hours of exposure. Many cases report symptoms in less than 12 hours with a few developing symptoms within 15 minutes of the initial immersion. This is in contrast to bacterially-induced rashes, which have a typical incubation period of greater than 24 hours, and sometimes up to a week. Of course the incubation period will vary according to the chemical concentration, the bacterial level, and the individual immune response, but a 24-hour cutoff applies to at least 90 percent of peer-reviewed cases published since 1980.

Table 1 – Comparison of rashes

Scientific literature has described numerous cases of rashes. Unfortunately most of the reports are incomplete. Most cases include good clinical information but fail to adequately describe conditions that led up to the outbreak. This should not be too surprising in that nearly all the cases are reported by clinicians rather than trained pool operators.

The published reports can be divided into three time periods: pre-1965, 1965 to 1982, and 1982 to present. Prior to 1965, rashes were linked to chlorine treatments. Reports of this type stop almost entirely around 1965. At that time, pool operators changed two factors: the concentration of free chlorine used in the water and how they measured chlorine. The current practice of maintaining 1 to 4 ppm free chlorine (and higher in some localities) began in the mid-1960s. At the same time, the preferred test method switched to DPD. Prior to 1965 pools were marginally chlorinated with less than 1 ppm total chlorine and the measurement system was OTO. Since OTO cannot assay for free chlorine, we have no way of knowing what the free chlorine concentration was. From what we know today about disinfection by-products (organic chloramines), we can safely conclude that concentrations of combined chlorine in the water prior to 1965 must have been significant and that the combined chlorine was probably the cause of the rashes. In the mid 1980s there were two more technological changes that had a significant impact: the introduction of convenient bromine compounds and the widespread introduction of hot tubs. Since this time, most reports of chemical rashes have been linked to bromine-treated water.

The reports of rashes from bromine-treated water started not long after BCDMH was first introduced. The first report was from the UK (Rycroft and Penny. 1983. Dermatoses associated with brominated swimming pools. Brit Med J. 287: 462). Rycroft was a dermatologist, and Penny was an occupational physician and advisor to the Amateur Swimming Association with extensive contacts in the sport. Based on Penny’s observations, the number of swimmers’ rashes expanded greatly shortly after BCDMH was introduced. Because the case reports do not include details of water chemistry, the causative agent of the rashes is open for speculation. There have also been a number of cases of rashes associated with bromine in the United States. These have occurred in both pools and spas. In these cases the large-scale outbreaks are associated with poor water quality, including cloudy water and foam. The reports from the UK are generally reports of individual cases, whereas the U.S. reports deal with mass outbreaks.

The single largest group reporting chemical rashes is hydrotherapists (therapists providing therapy in aquatic settings). These individuals are exposed to chlorine- or bromine-treated water up to ten hours per week. The temperature and bather loading of these therapy pools resembles hot tubs. One Israeli study revealed that 45 percent of the 190 therapists surveyed developed skin disease after beginning work (Lazarov, Nevo, Pardo, and Froom. 2005. Self-reported skin disease in hydrotherapists working in swimming pools. Contact Dermatitis 53:327-331). The authors concluded that skin disease for hydrotherapists is an occupational hazard resulting from cumulative exposure.

It appears that we can divide rashes into sporadic reactions among the general population and outbreak-associated. The percent of the swimming public that experiences rashes while using a properly maintained pool or hot tub is not known — but it is not zero. Kelsall and Sim surveyed parents of Australian 10- to 17-year-olds who swam in a hand-dosed chlorine pool, a chlorine pool with an automatic feeder and ozonator, or a bromine-ozone treated pool (Kelsall and Sim. 2001. Skin irritation in users of brominated pools. Intern J of Environ Health Research. 11:29-40). They reported that 7.7 percent, 7.6 percent and 4.2 percent of the swimmers, respectively, developed a rash at least once within 24 hours of swimming. The water chemistry summary indicates that all three pools were well maintained. This is in sharp contrast to outbreaks where up to 100 percent of the pool or spa users develop rashes. In one outbreak that resulted in 17 documented cases, including 5 that required urgent treatment at a local emergency room, the water was foamy and “covered in a froth-like substance” prior to the outbreak (Woolf and Shannon. 1999. Reactive airways dysfunction and systemic complaints after mass exposure to bromine. Environ Health Perspectives 107:507-509). Many of the outbreak reports indicate similar poor water quality.

So what is the exact cause of chemical rashes? We don’t know. The published cases do not provide enough information on the treatment system being used by the facility or chemistry discovered during the incident investigation. We do know that hypobromous acid (the active portion in “bromine”) is a poor oxidizer when compared to hypochlorous acid (the active portion in “free chlorine”). We also know that hypobromous acid reacts with organic matter to form combined bromamines, just as free chlorine does. And bromamines and chloramines are known skin irritants. A further complication is that there is no readily available test to determine the concentration of combined bromamines. OTO and DPD kits measure only total bromine, which includes the free bromine and combined bromine.

Anecdotal evidence suggests that rashes of this type are more likely to occur in hot tubs than in pools. The increased number of users per gallon of water results in much higher concentrations of organic matter in hot tubs. As this organic matter accumulates, the clarity of the water decreases and the water has an increased tendency to foam. Hot tubs are particularly challenging because the water chemistry can change so rapidly. I suggest that operators and inspectors ask the following questions during an investigation involving hot tubs.

• When was the water last replaced?
• How many bathers have used the facility since the water was replaced?
• Is any supplemental oxidation being done beyond the routine addition of chlorine or bromine?
• How often is the supplemental oxidation applied?
• When was it last applied?
• How many bathers have been in the water since it was oxidized?
• Did any patrons notice foam, cloudy water, or “off” odors in the days or hours prior to the rash outbreak?
• What were the results of any special tests, such as for disinfection by-products or bromide ion concentration?

If we can gather this type of information and then share it among our operators, we should be able to develop more robust treatment systems that eliminate the nuisance rashes.

Best Practices to Reduce Chemical Rashes

• Maintain the proper sanitizer level at all times – this not only provides oxidation but also prevents bacterial growth, including Pseudomonas aeruginosa that will cause bacterial rashes.
• Maintain proper pH and alkalinity – improper pH has been linked to some irritant rashes.
• Use routine supplemental oxidation to reduce combined chloramines and bromamines. Supplemental treatments include quick-dissolving chlorine compounds (cal hypo, dichlor, granular trichlor, lithium hypo, and bleach), non chlorine shock-oxidizers (monopersulfate), and ozone. Supplemental oxidation is particularly important when using bromine compounds (BCDMH, DBDMH or sodium bromide).
• In spas, routinely replace the water. There are several guides available for this, including one from the APSP (visit APSP’s website at http://apsp.org/54/index.aspx for a free download of APSP’s complete Water Treatment Information Bulletins.)
• When the water appears cloudy or foamy, the facility should be closed at once.

These all seem rather obvious. Yet in reported cases one or more of these were not followed by the operator.

Selected references on chemically-induced rashes.

1. Basler, Basler, Palmer and Garcia. 2000. Special skin symptoms seen in swimmers. J Am Acad Dermatol. 43:299-305.
2. Eun, Lee, and Lee. 1984. Sodium hypochlorite dermatitis. Contact dermatitis 11:45.
3. Fitzgerald, Wilkinson, Bhaggose, Beck, and English. 1995. Contact Dermatitis 33:53.
4. Habets, Geursen-Reitsma, Stolz, and van Joost. 1986. Sensitization to sodium hypochlorite causing hand dermatitis. Contact dermatitis 15:140-142.
5. Hostynek, Patrick, Younger, and Maibach. 1989. Hypochlorite sensitivity in man. Contact dermatitis 20:32-37.
6. Hostynek, Wilhelm, Cua, and Maibach. 1990. Irritation factors of sodium hypochlorite in human skin. Contact dermatitis 23:316-324.
7. Hurst. 1991. Disinfection of drinking water, swimming pool water, and treated sewage effluents. In Block (ed.) Disinfection, Sterilization, and Preservation, 4th ed. Lea and Febiger, Philadelphia, PA.
8. Kelsall and Sim. 2001. Skin irritation in users of brominated pools. Intern J of Environ Health Research. 11:29-40.
9. Lazarov, Nevo, Pardo, and Froom. 2005. Self-reported skin disease in hydrotherapists working in swimming pools. Contact Dermatitis 53:327-331.
10. Loughney and Harrison. 1998. Irritant contact dermatitis due to 1-bromo-3-chloro-5, 5-dimethylhydantoin in a hydrotherapy pool. Occup Med 48:461-463.
11. Osmundsen. 1978. Contact dermatitis due to sodium hypochlorite. Contact dermatitis 4:177.
12. Penny. 1999. Contact dermatitis due to BCDMH in hydrotherapy pool. Occup Med 49:265-268.
13. Penny. 1991. Hydrotherapy pools of the future — the avoidance of health problems. J Hosp Infect 18:535-542.
14. Rycroft and Penny. 1983. Dermatoses associated with brominated swimming pools. Brit Med J. 287: 462.
15. Sasseville, Geoffrion and Lowry. 1999. Contact Dermatitis 41:347-348.
16. Sasseville and Moreau. 2004. Contact allergy to 1-bromo-3-chloro-5, 5-dimethylhydantoin in spa water. Contact Dermatitis 50:323-324.
17. Woolf and Shannon. 1999. Reactive airways dysfunction and systemic complaints after mass exposure to bromine. Environ Health Perspectives 107:507-509.

Roy Vore, Ph.D., Research Microbiologist
DuPont Chemical Solutions Enterprise

Dr. Vore is a senior microbiologist in the Clean and Disinfect Division of DuPont’s Chemical Solutions Enterprise. Over the last fifteen years he has concentrated most of his work in the microbiology of swimming pools and spas. Dr. Vore has over 30 scholarly papers and presentations on the microbiology of swimming pools and spas. He has been an active participant on the APSP’s Recreational Water Quality committee since 1996.

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