Interesting Study (Dissertation) on DBP's in indoor pools

[Retep]

To my knowledge this is the first extensive study which examined indoor pools in the USA .
It seems that finally attention is being paid on DBP's in order to protect public health.
For good reason the German regulation (DIN 19643) limits the amount of THM's at max. 20 microgram/l.
More and more European countries are adopting those tough German regulations ( which are already in effect
in Germany since the last 20 years or so ).
The study (23 Pools in the USA) found the average to be at 62 microgram/l.. . .
Recently ( last week) another study came out from Canada were 15 indoor pools were monitored and the average of
those were at 55 microgram/l - more or less in line with the US Pools.
Finally someone even took TOC readings as well (7.1 ppm average)

What is surprising is the fact that NSPF didn't really address this issue in their Pool and Spa Operator Hand Book
(edition 2009 - page 46). . It says . . ."Currently the risk to human health due to THM's in swimming pools is relatively low ".
Low ? Life guards, Pool personal, swimmers and everyone who is exposed to this environment have a much higher cancer rate
than the average population. THM in the water means THM in the air.
Perhaps NSPF should take a look at this study - NSPF also recommends ideal levels in pools should be between 2-4 ppm
(those levels are considered to be a "shock treatment " in Germany where the max. FAC is set at 0.60 ppm for public pools)
Again - there is (obviously) a link between high free chlorine levels and the formation of THM's.

Seems like there is some hope that Governments and Health Departments in North America start to wake up and set much tougher standards in the future for public pools.

Enjoy reading those 278 pages ->
http://etd.lib.clemson.edu/documents/12 ... _10627.pdf

 

[chem geek]

Re: Interesting Study (Dissertation) on DBP's in indoor pool

That's a great paper. There are others that have much smaller samples of pools in the U.S. (usually < 10 and often just 2 or 3) and look at certain subsets of DBPs, but nothing as comprehensive as what was done with this paper. Unfortunately, this paper didn't see if Cyanuric Acid (CYA) was used in any of the indoor pools. One can presume that it was not since generally it is recommended not to be used or is explicitly banned from indoor commercial/public pool use in most states. Nevertheless, it's always an issue when not explicitly tested since it prevents one from drawing specific conclusions about active chlorine levels.

The paper unfortunately gets some things very wrong. On page 15 he states the following

From the above equations of chlorine chemistry in water we can see that the gas form of elemental chlorine tends to decrease the pH, while the sodium and calcium hypochlorites tend to increase the pH. Thus in the management and operation of swimming pools it is critical to adjust pH for maintaining the disinfection action efficiency. An acidic pH conditioner is necessary when hypochlorite salts are dosed to the pool, while a basic pH conditioner is required in the case of using chlorine in the gas form.

where he completely ignores the acidic nature of chlorine usage/consumption that makes hypochlorite sources of chlorine closer to pH neutral if one has a sufficiently lowered TA level.

The largest nitrogenous component of sweat and urine is urea, but the primary disinfection by-product that it produces is nitrogen trichloride, though depending on the study it also produces some chloroform. I write more about how lower active chlorine levels lower the amount of nitrogen trichloride that is produced in this post. Ernest "Chip" Blatchley's paper Volatile Disinfection Byproduct Formation Resulting from Chlorination of Organic-Nitrogen Precursors in Swimming Pools describes how the chlorination of creatinine can produce nitrogen trichloride (via urea) and dichloromethylamine; the chlorination of L-histidine can produce dichloroacetonitrile, cyanogen chloride and some nitrogen trichloride and chloroform; and the chlorination of L-arginine can produce some nitrogen trichloride. His paper Volatile disinfection by-product analysis from chlorinated indoor swimming pools identified 11 volatile DBPs including the three inorganic chloramines (monochloramine, dichloramine, trichloramine), the four trihalomethanes (chloroform, dichlorobromomethane, dibromochloromethane, bromoform), cyanogen chloride, cyanogen bromide, dichloroacetylnitrile, and dichloromethylamine. He also wrote a paper on the Reaction Mechanism for Chlorination of Urea.

There are many other studies of pools (mostly indoor) that have been done including those I write about this post and in this thread.

One interesting possible source of disinfection by-products in pools with CYA could come from the slow chlorine oxidation of CYA as described in this post. The key to formation of trihalomethanes such as chloroform is having an intermediate of a methyl ketone that then forms chloroform via the haloform reaction. Fortunately, the intermediates in the oxidation of CYA (biuret and allophanate ion) are not methyl ketones, but not all chemical pathways have been identified. Unfortunately, I do not see any specific studies identifying any DBPs from the chlorine oxidation of CYA.

Back to his paper, he notes that the most likely largest source of THMs from sweat/urine is from citric acid though it looks like urea isn't far behind (especially from urine where it's concentration is very high). He also noted that though there is a chlorine concentration dependence on the amount of THMs that are formed, that this goes away once chlorine demand is satisfied after 5 days of reaction time. The problem with this observation is that this is not how a real pool works. There is a regular introduction of new chlorine demand so a proper analysis would look at the steady-state (for slower reactions) or short-term variation (for faster reactions). THMs are volatile so the steady-state would be reached when the level of THMs being produced in the pool equals their outgassing rate. The rate of creation of THMs is going to be roughly proportional to the active chlorine level such that one would expect that a lower active chlorine level would lead to a lower THM steady-state amount. Also, the study reaction rates are completely unrealistic given the use of 100 mg/L chlorine levels so that they would end up with 3-5 mg/L residual after 5 days of contact time. The tables show fairly rapid THM formation, but given the high initial chlorine level that isn't a surprise. The reality is that at pool chlorine concentrations, THM formation is slower than indicated. This means that lower active chlorine levels have a chance to produce THMs at a slower rate such that other processes removing THMs from the water including outgassing, water dilution, and coagulation/filtration of precursors have a chance to occur. Nevertheless, the chloroform levels in the pools he studied weren't, on average, that high where most were under the EPA 80 ppb drinking water limit for chloroform (though all were above the German 20 ppb standard). I've seen other studies where the typical chloroform levels were quite a bit higher.

Out of curiosity, I've been getting THM measurements for my pool water, but given their high cost at $130 each, I haven't had many samples taken. Nevertheless, so far I see that they vary a LOT depending on factors such as when during the season they are taken, but most especially where the samples are taken. In particular, if they are taken near a bather who has used sunscreen, they are very high (the highest was around 180 ppb but the bulk pool water away from a swimmer was usually much lower than that). Our tap water has TTHM of 30 ppb with chloroform at 18 ppb. This points to something I haven't seen anyone research -- the use of different sunscreens and their reactivity in chlorinated pools. Since such reactions occur close to the skin, I would think they are even more relevant than bulk pool water concentrations at least for the dermal route though the study indicates that the inhalation route is more relevant to risk. I've also noticed variation depending on amount of water exposure to air and our use of a pool cover probably contributes to increased TTHM levels (i.e. tends to make it more like an indoor pool in some respects and values right after cover opening tended to be higher than after a day with the the cover open, especially if water was aerated).

I think that using CYA in pools, including indoor pools, would let one get to very low active chlorine concentrations even below the German standards but unless this is combined with removal of organic precursors and especially removal of formed DBPs, then it won't do as much good. Such removal can be accomplished through a combination of aeration / air exchange, cogulation/filtration, and alternative oxidation processes (MPS, advanced oxidation such as boron-doped diamond electrolysis or other processes such as ozone and UV though they can have their own issues). This is especially important for indoor and high bather-load pools.

 

[Retep]

Re: Interesting Study (Dissertation) on DBP's in indoor pool

The paper unfortunately gets some things very wrong. On page 15 he states the following

From the above equations of chlorine chemistry in water we can see that the gas form of elemental chlorine tends to decrease the pH, while the sodium and calcium hypochlorites tend to increase the pH. Thus in the management and operation of swimming pools it is critical to adjust pH for maintaining the disinfection action efficiency. An acidic pH conditioner is necessary when hypochlorite salts are dosed to the pool, while a basic pH conditioner is required in the case of using chlorine in the gas form.

where he completely ignores the acidic nature of chlorine usage/consumption that makes hypochlorite sources of chlorine closer to pH neutral if one has a sufficiently lowered TA level.

Don't know what he got wrong there :?:
If using sodium or calcium hypochlorites it raises the pH , therefore it must be lowered by (for example) Hydrochloric Acid ,and if using chlorine gas (to put it in simple words), we need to add a base ( such as soda ash for example) in order to raise the pH.

What you are saying is that if the TA is low then hypochlorite sources of chlorine got an acidic nature.
Even if your TA is at 20 ppm and you are using a hypochlorite source your pH still will go up and you need to correct it ( less though as if your TA would be high).

I know you are an advocate for using CYA in indoor pools and -Yes- it would have been very interesting if one or more of those indoor pools would have been using CYA and the relation to THM's. Also it would have been interesting to see with which levels of FAC would have to be operated by still obtaining microbiological safe water.
As you could see in this study there were no tests made in terms of microbiology ( which was not the purpose of this study to begin with).
If you take a look at those charts which show you the average FAC I am almost certain the microbiology was ok in all those pools. They better be ok considering those high FAC levels.

This study clearly proves that the "North American " approach ( = very high chlorine ) to treat pool water is not the proper way to do it.
Proper water treatment starts with proper filtration. Something which got lost in the past 20 years or so. In the "good old days" public pools
used proper filters and proper filtration speeds.
Nowadays pools got problems with water and air quality . Then they thought Ozone is the magic bullet, nowadays you see more and more UV irradiation , just to find out that this approach raises THM's up to 390 % .
As long as there is not a completely "re-thinking" and strict new laws/regulations ,our public pools in North America will stay a dangerous chemical soup for years to come.
I bet that 99.9 % of public pools in the USA and Canada would be closed down immediately if the DIN 19643 would be applied .
Another scary thought is that in order to become a CPO all it takes is a 16 hour course and then the newly CPO is legally able to run a public
swimming pool where perhaps 1000 people visit this pool each and every day.
From what I have seen all the CPO's remember only one thing : pH of the human eye is 7.5, therefore they keep the pool water at 7.5.
And if the Saturation Index or Langelier Index is followed and balances then the Pool is "perfect".
Very scary.

 

[Retep]

Re: Interesting Study (Dissertation) on DBP's in indoor pool

Nevertheless, the chloroform levels in the pools he studied weren't, on average, that high where most were under the EPA 80 ppb drinking water limit for chloroform (though all were above the German 20 ppb standard). I've seen other studies where the typical chloroform levels were quite a bit higher.

The risk of exposure to THM's in pool water is about 93 times ( ninety three) higher than exposure by tab water ingestion !
( B.Levesque and Agazotti study)
In other words - you could drink tab water up to 80 ppb of THM and the cancer risk is relatively low.
THM in pool water is quite a different story since THM's are volatile (out gassing) - and that's where the swimmer is breathing it in.
The lungs are absorbing it like a sponge and THM levels in the blood increase like mad.
On top of it you got the dermal exposure as well .
32 ppb is considered to be already "slightly contaminated" ( Agazotti study).
The last few pages of the previous linked 278 page study (Dissertation) ,shows a few models in term of expected cancer rates when people are exposed to THM's in pool water.
To my knowledge ( can't confirm it yet), one Province in Canada will come out with new regulations , where they will set a maximum level of Chloroform (part of the THM family) in the pool water. Why they don't take TTHM's is a mystery to me, but at least it's a good start.
Apparently they will set the maximum at 40 ppb , progressively lowering it over the next few years. FAC max. of 1 ppm and as low as 0.50 ppm providing parameters in terms of microbiology are met.
Also regulations for air quality will be in effect as well - Trichloramines in the air should not exceed 0.50 ppm/m3.( in 2010 France proposed 0.30 ppm/m3 - it is still under review).
That would be a first in North America and if they really follow it through they should be congratulated.

I recently downloaded another study, which came out from Canada - just got released about 3 weeks ago and I purchased it online ( too bad not everything is free on the net. . .)
Only 40 pages long this time.
Here is the link ->
http://www.sciencedirect.com/science/ar ... 5411003903

 

[chem geek]

Re: Interesting Study (Dissertation) on DBP's in indoor pool

If using sodium or calcium hypochlorites it raises the pH , therefore it must be lowered by (for example) Hydrochloric Acid ,and if using chlorine gas (to put it in simple words), we need to add a base ( such as soda ash for example) in order to raise the pH.

What you are saying is that if the TA is low then hypochlorite sources of chlorine got an acidic nature.
Even if your TA is at 20 ppm and you are using a hypochlorite source your pH still will go up and you need to correct it ( less though as if your TA would be high).

There are quite a few pool owners using hypochlorite sources of chlorine who add little or no acid. There are even some spa users using bleach (after initial Dichlor) who likewise have stable pH. Though it is true that there is usually the tendency for the pH to rise when using hypochlorite, if the TA is low enough then the amount of needed acid gets very low and the TA need not get to 20 for that to happen (you can still be over-carbonated and have very little outgassing since the rate is proportional to the square of TA and is not linear). I am not saying that "hypochlorite sources of chlorine got an acidic nature". The usage/consumption of chlorine from ANY source is acidic and it exactly counteracts the pH rise from hypochlorite sources being added except for the "excess lye" in such sources which can be very low (in Clorox bleach at a pH of 11.9 it's 0.063% sodium hydroxide). This effect makes Dichlor net acidic and Trichlor even more acidic than it is upon addition. See this post for the chemistry.

I know you are an advocate for using CYA in indoor pools and -Yes- it would have been very interesting if one or more of those indoor pools would have been using CYA and the relation to THM's. Also it would have been interesting to see with which levels of FAC would have to be operated by still obtaining microbiological safe water.
As you could see in this study there were no tests made in terms of microbiology ( which was not the purpose of this study to begin with).
If you take a look at those charts which show you the average FAC I am almost certain the microbiology was ok in all those pools. They better be ok considering those high FAC levels.

I don't think there's any problem with bacteriological safety even with relatively low active chlorine levels. The German DIN 19643 at 0.3 without ozone or 0.2 with ozone is still more than enough and remember that its pH is lower as well (around 7.0) so with no CYA present the active chlorine level is about 50% higher than at 7.5. If CYA is present and the FC is at 20% of the CYA level, then this is equivalent to 0.2 ppm FC with no CYA at 7.5. I just think of CYA as a useful chlorine buffer to make the active chlorine level lower while still having plenty in reserve while also protecting it from breakdown in sunlight. It should at least be considered. It won't work with DIN 19643 economically, however, due to the GAC chlorine adsorption/stripping that is part of that system -- that is, chlorine is removed with every turnover and reinjected (at least in some versions -- I've heard inconsistent reports about when GAC has to be used).

The thing you need to keep in mind is that CYA is used in most outdoor pools in the U.S. so the active chlorine level is lower in such pools -- lower than the lowest of German DIN 19643. Most studies have been with indoor pools and the presumption has been that the difference in air circulation explains the differences seen, but sunlight exposure and the use of CYA may also be factors, but aren't generally considered. Even if a pool had 10 ppm FC, that means nothing to me if I don't know the CYA level. If the CYA is 100 ppm, then the hypochlorous acid level is still much lower than the lowest of 19643.

This study clearly proves that the "North American " approach ( = very high chlorine ) to treat pool water is not the proper way to do it.
Proper water treatment starts with proper filtration. Something which got lost in the past 20 years or so. In the "good old days" public pools
used proper filters and proper filtration speeds.

I agree that having a high active chlorine level as with typical North American indoor pools with no CYA is a problem as is the tendency to shock those pools to even higher chlorine levels in an attempt to chase CC to get it lower. Of all the problems, CC is actually the least to worry about if one uses CYA in pools. The reason is that the low active chlorine level should lower the amount of nitrogen trichloride produced by orders of magnitude. However, the CC may measure higher because most of it will be intermediates such as monochloramine and chlororureas that are not a problem even at 1 ppm. Even 19643 focuses on lowering CC, but that's more of a marker for general precursor removal including urea and therefore a proxy for nitrogen trichloride (the reality is that most European pools don't get to 0.2 or 0.3 and operate closer to 0.5 ppm since it's hard to maintain such a low FC level -- yet another reason why CYA could be helpful).

I also agree that very few, if any, pools in North America would pass German DIN 19643. Of course, they aren't using that standard so that's not really a surprise.

I agree that there should be more focus on coagulation/filtration. On the other hand, I'm even more concerned with the suntan lotion effect I saw in my own pool since there are many more users of outdoor pools and nearly everyone uses sunscreen these days. I'm doing more tests hoping that was just an anomaly (even then, what I'm doing is hardly a real scientific controlled experiment).

The last few pages of the previous linked 278 page study (Dissertation) ,shows a few models in term of expected cancer rates when people are exposed to THM's in pool water.
:
I recently downloaded another study, which came out from Canada - just got released about 3 weeks ago and I purchased it online ( too bad not everything is free on the net. . .)

Most studies show that it isn't drinking tap water that is the primary exposure route, but rather dermal and mostly inhalation exposure. That's why showering is also a significant factor though indoor swimming is higher and why competitive swimmers are at greater risk than casual bathers.

Yes, it's good of Canada to take a stab at this, but they will find that maintaining lower FC levels is difficult since even small localized events can wipe out FC. So while 0.5 ppm may be doable with sufficient circulation and monitoring, getting to 0.2 or 0.3 will be more difficult. Again, I think CYA would help here significantly.

Thanks for the additional link. Yes, it's too bad that many of these papers have to be purchased and I've bought many.

I want to put into perspective a few things. First, this dissertation study didn't measure actual air concentrations nor blood levels. Though he wrote that his Henry Law estimates compare well with other studies, there are some where such near-saturation assumptions don't seem to work well and where blood levels aren't as high as would otherwise be expected. This study is an earlier one showing indoor pools as being more of a problem for the inhalation route of chloroform in terms of blood levels that didn't show up in outdoor pools, but amounts do not follow simplistic Henry's Law calculations and there were no hepatotoxic effects seen. The Spanish studies I looked at even showed that chloroform was not genotoxic. So I don't believe it's such a slam dunk that chloroform in particular is as serious a health issue at these levels though it is a marker for TTHM which is useful since the brominated THMs have been shown to be far more problematic.

These risks which are projected with linear dose models and have conservative margins of error should be compared against actual lifetime cancer risk from all sources as listed in this link. The dissertation showed risks 10 to 10,000 times higher than the 1 in a million EPA unacceptability limit making the worst-case 1 in 100. That's pretty bad if it were true, but it's unlikely to be that high since epidemiological studies don't show such high increases (and some such as this bladder cancer study have potential flaws). The risk is more likely to be more like 10 times higher so in the 1 in 100,000 range as that is more consistent with other studies that measured more direct physiological effects, though again it's not clear that chloroform is indeed the culprit and the brominated THMs and other factors (nitrosamines) may be more at play.

I'm not saying that this isn't something to improve, but I don't believe it's something to get panicked about either. The risk in outdoor residential pools should be a lot lower, notwithstanding the suntan lotion issue I seem to have stumbled upon.

 

[Retep]

Re: Interesting Study (Dissertation) on DBP's in indoor pool

There is probably nothing to panic about when you swim in an outdoor Pool - I do agree with you.
Problematic is in the indoor pools and especially for the people who spend lots of time in the enclosed Pool environment.

Basically the tough German laws came into effect when the Germans found out ( in the mid 70' or so ) , that the lifeguards and personal who worked in the pool environment all day long ,had an unusual high rate of health problems compared with the general public.
As a consequence the Government/ Health department took notice and that was the "birth" of the DIN 19643 regulation.
Quite a bit of opposition of first (as any new regulation/ change ) , but since then nobody questions those regulations.

 

[loop_pea]

Re: Interesting Study (Dissertation) on DBP's in indoor pool

I don't think there's any problem with bacteriological safety even with relatively low active chlorine levels.

In your excel spreadsheet (and elsewhere) you quote a minimum of 0.011 ppm HOCl for sanitation. This would not be achieved in a pool with pH of 7.5, FC of 3.0 and CYA of 150. Yet this is permitted under UK guidelines. I see a possible problem here, and this is behind some of my recent comments about the CDC not taking on board the link between CYA level and kill times.

 

[ivyleager]

Re: Interesting Study (Dissertation) on DBP's in indoor pool

(At times like these and when reading these discussion I realize my brain has quite a bit of wasted potential).

 

[chem geek]

Re: Interesting Study (Dissertation) on DBP's in indoor pool

Well, yes, I should have been more specific when I wrote "relatively low active chlorine levels". There's a spectrum of risk, but the 0.011 ppm HOCl is lower than what would be reasonable to prevent person-to-person transmission. That low level is more to prevent uncontrolled bacterial growth for fecal bacteria and other relatively easy-to-kill bacteria. A more reasonable level for commercial/public pools would be in the 0.1 ppm FC or perhaps 0.2 ppm FC equivalent with no CYA, so roughly an FC that is 10-20% of the CYA level. For residential pools, the lower levels that prevent algae growth are fine -- FC that is 5% of the CYA level for SWG pools, for example.

So yes, I agree with you on the low FC/CYA ratios in commercial/public pools being yet another issue, but in practice it doesn't seem to be a pressing issue -- more of a theoretical one. Outbreaks are easier to detect and can occur when there is uncontrolled bacterial growth. Having just a nearby person get sick from person-to-person transmission of a virus (for example) due to too low an active chlorine level is much less likely to get reported let alone associated with swimming. That's why APSP-11 says the following:

The effect of cyanuric acid on oxidation of organics, kill rates of bacteria and viruses, algae, and protozoa has been demonstrated. Some authorities or standards have suggested adjusting the required chlorine residual to the concentration of cyanuric acid to compensate for the reduction in rates of kill. These studies are not fully comprehensive and applicability to real pools has not been demonstrated. Specifically, we do not have any empirical evidence that a disease outbreak has been linked to a particular cyanuric acid level in a properly sanitized pool (i.e., when at least 1 ppm free available chlorine was present in the pool).

It's sort of a "well, nobody died" argument, nevertheless I was unable to convince anyone otherwise, but then again I wasn't on the committee. The chairman of the committee worked for Chemtura when the committee started. Chemtura sells stabilized chlorine and does not sell unstabilized chlorine (unlike Arch Chemicals who also sell Cal-Hypo). A member of Arch was also on the committee.

 

[Retep]

Re: Interesting Study (Dissertation) on DBP's in indoor pool

A member of Arch was also on the committee.

Typically.
Take a look at the members of the so called "advisory committee"and "Board of Directors" of NSPF.
I do suspect it is not in their commercial interest to "lower down " suggested FAC levels in public pools.
Basically the same thing ( 2-4 ppm) is being preached since the last 30 years. . . .
If there was a "committee" of a health department / agency , none of those people should be on it.
Take really scientists who have absolutely no connections to any kind of any manufacturers.
NSPF is a private enterprise. Nothing more, nothing less.

 

[chem geek]

Re: Interesting Study (Dissertation) on DBP's in indoor pool

I think it's more inertia than anything else. There are nearly 10 million residential pools in the U.S., but only 1 million commercial/public pools. The main business for the chlorinated cyanurates and even Cal-Hypo is the residential market. Commercial/public pools with their heavier bather loads couldn't use these products or else the CYA and CH would get too high too quickly (yes, some commercial pools use them, but generally only with lower bather loads).

Even in Europe, the DIN 19643 standard is for commercial/public pools and most residential pools don't follow it, mostly because it's a lot more expensive to do so and with their lower bather loads and mostly being outdoor pools there is less of a need. Having commercial/public pools in North America, especially indoor ones, move to tighter standards isn't really going to affect the economics at the chemical manufacturer/distributor companies so I don't believe that's why they are slow to change. It really does just seem like inertia -- a general resistance to change. But we can just choose to agree to disagree on this point.

 

[loop_pea]

Re: Interesting Study (Dissertation) on DBP's in indoor pool

Well, yes, I should have been more specific when I wrote "relatively low active chlorine levels".

Ah, being specific is the bane of the pool industry. I've received a lot of advice, some of it conflicting, and most of it wasn't so much wrong as simply out of context.

There's a spectrum of risk, but the 0.011 ppm HOCl is lower than what would be reasonable to prevent person-to-person transmission. That low level is more to prevent uncontrolled bacterial growth for fecal bacteria and other relatively easy-to-kill bacteria.

This begs the question, what is a safe minimum HOCl level for uncontrolled bacterial growth and for keeping kill times down to prevent person to person transmission?

I wandered into this thread originally because of the discussion of DBPs, and I wanted to add my two cents. When using very low active chlorine levels, production of DBPs goes way up. So the studies that claim higher levels of chlorine increase production of DBPs are not wrong but the context is indoor pools not using CYA. I guess that context is pretty clear from the title of the thread; but I bet people in the industry will try to apply this logic to outdoor pools using CYA, and I don't think it's valid.

In pools using CYA you would be hard pushed to get to the high active chlorine levels being talked about in these studies. Even at shock levels the active chlorine concentration is less than in a pool with no CYA and 5ppm FC (is that right?). I would have thought the average outdoor pool owner is more likely to encounter the opposite problem of not enough chlorine giving rise to a pool smell. That's all too easy to do when simply following local guidelines (we've been there, done that and got the T-shirt). Increasing FC levels then helps to reduce, not increase, DBPs.

Am I making sense?

 

[chem geek]

Re: Interesting Study (Dissertation) on DBP's in indoor pool

This begs the question, what is a safe minimum HOCl level for uncontrolled bacterial growth and for keeping kill times down to prevent person to person transmission?

The answer isn't simple because it depends on the specific pathogen you are trying to control and on what one would consider to be a reasonable kill rate in what time to prevent person-to-person transmission. In this post I roughly normalized the times for a 99.9% kill (3-log reduction) of various pathogens when the FC was roughly 10% of the CYA level equivalent to 0.1 ppm FC with no CYA in terms of active chlorine level. Preventing uncontrolled bacterial growth means killing 50% of the bacteria faster than the time it takes for them to double in population (i.e. the generation time). A 1 minute kill time for a 3-log reduction at 0.1 ppm FC translates to around 0.008 ppm FC (with no CYA) for a 50% kill in 15 minutes. 0.008 ppm is a very low level of chlorine though is about what is found with 1 ppm FC with 100 ppm CYA.

Some standards such as EPA DIS/TSS-12 are pretty ridiculous because they require a 99.9999% kill (6-log reduction) of Escherichia coli and Enterococcus faecalis (used to be classified as Streptococcus faecalis) in 30 seconds or less. Basically, this requirement is roughly equivalent to requiring 0.4 ppm FC with no CYA (at pH 7.5). The irony is that 1 ppm FC of Dichlor or Trichlor with only 2 ppm or higher CYA would fail this test. It is only because Dichlor and Trichlor are tested in water free of CYA (except for that added by the Dichlor or Trichlor itself) that they are able to pass.

German DIN 19643 is essentially the same requiring a 99.99% kill (4-log reduction) of Pseudomonas aeruginosa within 30 seconds where this bacteria is a little slower to kill. The FC is expected to be from 0.3 to 0.6 ppm with a pH from 6.5 to 7.2. Note the lower pH intended to reduce THM formation. I wonder how they keep the pH so low -- is the TA kept low as well and if so is the CH very high to protect plaster surfaces? Is equipment beefed up to avoid corrosion (e.g. cupro-nickel or titanium heat exchangers instead of copper)?

I think these standards are a little too stringent, but that partly comes from the fact that they are based on not having CYA in the water. It is hard to control chlorine levels of 0.05 to 0.2 ppm where such low capacities could be readily exhausted in bacterial challenge tests. Though the kill times would indeed be slower, they wouldn't be terribly slow and the CYA would allow for ample buffering of plenty of chlorine to handle local depletion from bather events (even urinating children). 4 ppm FC with 20 ppm CYA would be roughly equivalent to 0.2 ppm FC with no CYA at pH 7.5.

I wandered into this thread originally because of the discussion of DBPs, and I wanted to add my two cents. When using very low active chlorine levels, production of DBPs goes way up. So the studies that claim higher levels of chlorine increase production of DBPs are not wrong but the context is pools not using CYA. In pools using CYA (I suspect that's most people on this forum) you would be hard pushed to get to the high active chlorine levels being talked about. Even at shock levels the active chlorine concentration is less than in a pool with no CYA and 5ppm FC (is that right?).

I would have thought that public or semi public pools using CYA (outdoor pools) are more likely to encounter the opposite problem of not enough chlorine giving rise to a pool smell. That's all too easy to do when simply following local guidelines (we've been there, done that and got the T-shirt). Increasing FC levels then helps to reduce, not increase, DBPs in that situation.

You are right that in pools using CYA the active chlorine levels are generally low. For this forum, the SWG pools have the same active chlorine level as pools with 0.04 ppm FC and no CYA while the non-SWG pools have at least 0.06 ppm FC with no CYA. Shock level is equivalent to 0.6 ppm FC with no CYA while yellow/mustard shock level is equivalent to 1.5 ppm FC with no CYA.

I think we need to be more specific about the DBPs because at low active chlorine levels the rate of production of DBPs is slower but the buildup of some of them can be higher. At lower active chlorine levels, all reactions with active chlorine (hypochorous acid) are slower. The good news is that this means that the initial DBP formation is slower. However, what happens longer-term depends on the specific intermediates that are produced and with what happens to the final products. The idea that "too little chlorine" leads to higher DBPs is mostly referring to the inorganic chloramines because the oxidation of ammonia is slowed down at lower active chlorine levels. Ammonia still quickly becomes monochloramine, but there is a build-up of monochloramine and dichloramine for a longer period of time though on the plus side the nitrogen trichloride amount is lower. There is a balance or trade-off between these and I believe the sweet spot at higher bather loads is around 0.2 ppm FC with no CYA though some could argue it's somewhat higher.

The thing is that monochloramine really isn't particularly offensive until it gets to higher levels. Many water supplies now use chloramination and my own water supply has 1.2 ppm monochloramine yet does not smell offensive. The odor threshold for dichloramine is in the 0.1 to 0.5 ppm range, but nitrogen trichloride is offensive and irritating starting at 0.02 ppm (20 ppb). As shown in this post, using CYA in the water to achieve a low active chlorine level can balance between these three to keep the nitrogen trichloride down low. The German DIN 19643 has a low-ish active chlorine level at the low-end of its range, but it's pH is low so can still produce nitrogen trichloride above the odor threshold and yet have a low CC. So ironically, CC is not necessarily a good factor for determining air quality. It is only in the extremes of too low an active chlorine level or when running out of chlorine when the CC > 0.2 ppm can become a problem (and yes, a much higher CC can still be noticeable on its own). A higher CC can also indicate high amounts of organics such as urea showing up as chlorourea, but again a level above 0.2 ppm is not necessarily a problem though higher levels may be, depending on the active chlorine level.

You should be aware that another driving force towards the tendency in the U.S. to have high active chlorine levels comes from Kent Williams of PPOA as seen through articles on oxidation and CYA, and ORP. His background is from Stranco, a manufacturer of ORP controllers (since purchased by Siemens). The argument is that one needs high active chlorine levels to provide sufficient oxidation power to oxidize bather waste quickly enough. The side effects of faster oxidation of swimsuits, skin and hair, faster corrosion of equipment, and faster creation of DBPs (and larger amount of nitrogen trichloride) are not usually discussed. For high bather-load pools, especially indoors without the help of UV from sunlight creating hydroxyl radicals from chlorine, I believe that having a lower active chlorine level usually requires supplemental oxidation or coagulation/filtration to handle the bather waste. Even indoor residential pools often require some form of supplemental oxidation to improve air quality (UV is most commonly used). Advanced oxidation processes such as the use of boron-doped electrodes in electrolysis to produce hydroxyl radicals as in Oxineo® is a possibility.