WARNING: TECHNICAL POST (skip if not interested)
There are three somewhat related papers all released around the same time and I'll write about each below. Do not be scared by this. Outdoor residential pools are low in bather load, are generally exposed to UV in sunlight, have good air circulation, and use CYA in the water. All of these factors should lower DBPs by a huge amount (at least a 10x reduction if not more).
Genotoxic Effects in Swimmers Exposed to Disinfection By-Products in Indoor Swimming Pools
For
this genotoxicity paper, the most amazing thing is that they did not use a control of people swimming in a pool without chlorine or doing similar physical exercise. Other studies (see below) at least measured disinfection by-products (DBPs) in the water and air and in exhaled breath before and after swimming, but measuring other body chemistry factors without using a control does not separate out exposure to pool air from exercise. Nevertheless, it's probably reasonable to assume that their genotoxic results are due to DBP exposure -- it just would be better to have a control to confirm this since increased metabolic rates also increase genotoxicity. That's why very low calorie diets lead to long life extension (in animals, anyway) since metabolism increases the levels of the body's own mutagenic chemicals including free radicals. The authors did mention other studies showing more direct correlations.
This study showed the same result as the last one below in terms of measured THMs being much higher in breath after swimming. It should be noted that chloroform is not genotoxic, but
the other THMs (all of which have bromine) are genotoxic and that the pools studied have higher bromide levels in their fill water.
Swimming was not associated with DNA damage.
What's in the Pool? A Comprehensive Identification of Disinfection By-Products and Assessment of Mutagenicity of Chlorinated and Brominated Swimming Pool Water
More details of a related study are
here at CREAL. The actual published paper of this additional study is at
here.
They used the DPD test to determine Free Chlorine (FC), monochloramine, dichloramine, trichloramine. However, Dr. Ernest "Chip" Blatchley's work using MIMS technology has shown that DPD does not correctly measure chloramines. Some form of chlorourea will show up as dichloramine, for example. The study noted that a smaller number of disinfection by-products (DBPs) is found in studies of outdoor pools, most likely due to the greater air circulation and exposure to sunlight in outdoor pools as many DBPs are volatile and photolyzed (broken down by the UV in sunlight). Their average chlorine level was 1.28 ppm (most likely with no CYA) while monochloramine was 0.29 and dichloramine (which is more likely to be a chlorourea) was 0.38 for the chlorinated pool. To their credit, the study does note "as DPD analysis of chloramines cannot differentiate organic from inorganic forms of these compounds, it would be possible that these levels are overestimated by the occurence [sic] of organic chloramines in the swimming pool waters." They then refer to one of my favorite studies, the breakpoint chlorination model of Jafvert and Valentine (1992). They also refer to membrane-introduction mass spectrometry (MIMS) and note similar levels as found by Blatchley, though the papers I've seen of his have shown much lower true dichloramine levels.
The mutagenecity of the swimming pool water was similar to that of treated drinking water. It's toxicity to microorganisms is higher (even though samples were dechlorinated) so the highest mutagenic dose for the pool water is limited compared to that of drinking water.
Short-Term Changes in Respiratory Biomarkers after Swimming in a Chlorinated Pool
There was a related study by the same main authors
here. Amazingly, though the researchers measured lung biomarkers before and after swimming in an indoor chlorinated pool, they did not measure the same thing in swimming in a non-chlorinated pool (i.e. they didn't have controls) to make sure that it wasn't the exercise of swimming that increased the biomarkers, though the tests for DBPs were still relevant (unless the body were to produce those which is highly unlikely). For example, they did measure the four trihalomethanes (THMs), chloroform, bromodichloromethane, dibromochloromethane and bromoform in the participant's breath before and after swimming. They also measured Free Chlorine (FC), THMs, mono, di and trichloramine in the pool water. In this study as well they used the DPD test for chloramines. Indoor air was also sampled for THMs.
The average FC level was 1.17 mg/L and I would presume that there was no Cyanuric Acid (CYA) in the water. The average dichloramine reading (they imply that the monochloramine reading was similar) was 0.43 mg/L.
The result was that the THMs in exhaled breath rose by a factor of 7 on average after swimming.
CONCLUSION
Remember that these are indoor high bather load pools. The amount of DBPs in virtually every study made is correlated with bather load. Also, lower levels are found in outdoor pools than indoor pools most likely due to greater air circulation and exposure to the UV in sunlight, but also for pools that use CYA the nitrogen trichloride level should be lower (in theory, maybe even the THMs to some degree). Finally, the worst DBPs tend to be the brominated organics (including THMs) so a chlorinated pool will tend to have lower quantities of such DBPs than a bromine pool unless the fill water is high in bromide (as in the pools in their studies in Barcelona, Spain) or one is using sodium bromide algaecide (which essentially turns the pool into a bromine pool).
I believe the easiest way for commercial/public high bather load pools to minimize the DBPs is to use a lower active chlorine level by using CYA in the water to achieve the equivalent of 0.1 to 0.2 ppm FC with no CYA and to also use supplemental oxidation (UV, ozone, non-chlorine shock MPS, enzymes). In fact, these go hand-in-hand since the lower active chlorine level gives precursor molecules more time to be exposed to the supplemental oxidizers and also gives them more time to volatize before reacting with chlorine.
By comparison, the FC level relative to the CYA level proposed on this forum has an active chlorine level that is well over 10 times lower (equiv. FC with no CYA of 0.06 - 0.1) than found in the studied pools (FC of 1.2 with no CYA). The bather load is also likely to be at least 5-10 times lower. More detailed calculations on this are in
this post.
Richard
.
