This article seems thinly researched to me, and I am wondering why they don't link the cancer risk to chlorinated drinking water systems. I have tested water in my lab before and found the tap water from our sink was more highly chlorinated than the swimming pool water I was testing.
What are your thoughts on this article, and is APSP responding to this one? It seems to me this is very bad press for our indsutry and likely to be faulty science as well. Is the group doing this research an environmental group with an agenda? I find this very suspect. I'd be interested in knowing what everyone thinks about this article. It has been linked on the Drudge Report for several days.
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So your customers must have been referring to some earlier studies since they brought up concerns years ago, possibly something like this asthma study published in 2003 or this one from 2008 (I write about these studies in this thread. Or if it was specifically about cancer, then there is this study published online in 2006 linking chlorination disinfection by-products to an increase in bladder cancer. This last study (which is an epidemiological survey like the asthma studies, not an experiment like the ) basically showed a doubling of the risk of bladder cancer at 50 µg/liter THM levels with somewhat higher risk from showering, bathing and swimming than from drinking water (though the risk doubling is from total exposure, most of that being from showering). Sudies of commercial/public swimming pools often show 50-100 µg/liter THMs where outdoor residential swimming pool THMs would be expected to be far lower. In the U.S., there are around 70,000 new bladder cancer causes each year with around 15,000 deaths. Interestingly, the National Cancer Institute does not list chlorinated DBPs as associated with bladder cancer.
The bottom line is that yes, people do believe these articles, even the educated ones. Our message must get out there in a big way to counter the pseudo-science.
One should look at Table 2 in the study since it sums up what was observed overall. When looking at mean values of biomarkers for the four tests that were done, the only statistically significant result was a DECREASE in actual measured DNA damage in the comet assay. That is, the swimming overall on average doesn't point to any significant conclusion with regard to DNA damage, micronucleation or mutagenicity. The other study conclusions that were statistically significant have to do with correlations of changes with measured exposure levels of THMs in breath as shown in Table 3. This is where there was no significant correlation with any of the THMs for actual DNA damage so the statistically significant decrease (from 1.5 +/- 0.7 to 1.3 +/- 0.6) that was seen may have been due to the exercise itself (I'm speculating here). There was no statistically significant correlation with THMs and the micronucleated urothelial cells test. For the micronucleated lymhpocyte test, there was correlation only with the brominated THMs though on average the increase that was seen was from 3.4 +/- 2.4 to 4.0 +/- 2.8. For the urine mutagenicity test, only bromoform showed a statistically significant correlation (remember that this test showed the average doubling).
As for how the people were using the pool, this was a controlled study so 49 non-smoking adult volunteers aged 18 to 50 who were asked to swim for 40 minutes in the indoor chlorinated pool. They were requested not to swim for one week prior to the experiment. There was a lot of variation in the actual distance swam during those 40 minutes from 0.05 to 1.75 kilometers (average 0.90 +/- 0.4 standard deviation). They did micronuclei and DNA damage tests on blood lymphocytes taken before and 1 hour after swimming. They did micronuclei tests of exfoliated urothelial cells before and 2 weeks after swimming. They did urine mutagenicity tests before and 2 hours after swimming.
In the study, they note that "Physical activity has been shown in some studies (Schiffl et al. 1997) to be associated with genotoxicity through an effect on oxidative stress, but the results are not consistent (Battershill et al. 2008; Stephanie et al. 2008). In our study population, adjustment in the analysis for the intensity of physical activity during swimming did not confound effect estimates for exposures to DBPs." I still wish that they had used a control pool with low bather load and minimal DBPs.
For example, in their genotoxic study, they note that "swimming was not associated with DNA damage detectable by the comet assay." So far, so good, though this would not catch DNA damage that was subsequently repaired. They also note that "no significant associations with changes in micronucleated urothelial cells were observed." Also good, since that is a biomarker of DNA repair. However, they note that "the change in the frequency of micronucleated lymphocytes after swimming increased in association with exhaled concentrations of the brominated trihalomethanes (p=0.03 for CHCl2Br, p=0.05 for CHClBr2, p=0.01 for CHBr3) but not for chloroform" and that "urine mutagenecity increased significantly after swimming in association with the concentration of exhaled CHBr3 (p = 0.004)." Gee, that doesn't sound good, but wait...
If we look at urine mutagenecity, it went from 0.6 +/- 2.3 to 1.2 +/- 2.2 Rev/ml-eq where the fraction of variance explained by exposure to THMs was only statistically significant with bromoform and even then that fraction was only 16% -- that is, most of the increase might be due to exercise itself (or from some substance not measured). If we look at the micronucleated lymphocytes, they increased only from 3.4 +/-2.4 to 4.0 +/- 2.8. In their text, they consider the micronucleated cell increases to be have increased non-significantly so I don't know why they bothered to refer to the non-significant increase that they associated with the brominated trihalomethanes in their "RESULTS" section.
So the only really significant finding here was the factor of 7 increase in trihalomethanes (THMs) in the breath after swimming since it can be reasonably assumed that this did not come from exercise alone. However, the net result of this increase in terms of affects on the body that they looked at were only partially attributable to that increase in THMs (specifically to bromoform and to a lesser extent the other brominated THMs) and could instead be mostly attributable to exercise itself, possibly due to increased metabolic rates since increased metabolism and breathing results in greater intake of oxygen and associated free radical formation which can increase the rates of mutations.
In practice, exercise is healthy in many ways, but it is "accelerated living" which may result in increased DNA damage which is mostly repaired. That is, it's a part of life and the benefits of exercise (such as improved cardiovascular health) outweigh the downside risk (such as DNA damage that is not repaired and on rare occasions could be cancerous). The opposite of this effect is the long life extension found by putting rats and other animals on significantly calorie-restricted diets. Slower metabolism means slower mutation rates and aging in general (telomere shortening, etc.), but a pretty sluggish life.
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