Gabriella Aggazzotti, Department of Sciences of Public Health, University of Modena and Reggio Emilia, Italy
Guglielmina Fantuzzi, Department of Sciences of Public Health, University of Modena and Reggio Emilia, Italy
Elena Righi, Department of Sciences of Public Health, University of Modena and Reggio Emilia, Italy
Guerrino Predieri, Department of Sciences of Public Health, University of Modena and Reggio Emilia, Italy
Pierluigi Giacobazzi, Department of Sciences of Public Health, University of Modena and Reggio Emilia, Italy
Petra Bechtold, Department of Sciences of Public Health, University of Modena and Reggio Emilia, Italy
Katia Mastroianni, Department of Sciences of Public Health, University of Modena and Reggio Emilia, Italy
Background and Aims: The aim of this cross-sectional study was to investigate the association between airborne NCl3
exposure in indoor swimming pools and the prevalence of self-reported respiratory and ocular symptoms in occupationally
exposed subjects.
Methods: Twenty indoor swimming pools in the Emilia-Romagna region of Italy were included in the study. Information about
the health status of 128 employees was collected using a self-administered questionnaire. Exposure to airborne NCl3 was
evaluated in indoor swimming pools by a modified DPD/KI method.
Results: The airborne NCl3 levels ranged from 204 to 1020 µg/m3
with a mean value of 648.7 ± 201.4 µg/m3
. More than 50% of
the swimming pools showed airborne NCl3 levels higher than 500 µg/m3
(recommended WHO guidelines). Both ocular and
upper respiratory symptoms were very frequent in the 128 employees: red eyes, runny nose, voice loss and cold symptoms
were declared more frequently by pool attendants (lifeguards and trainers) when compared with employees working in other
areas of the facility (office, cafe, etc.). Pool attendants exposed to airborne NCl3 levels higher than 500 µg/m3
higher risks for runny nose (OR: 2.9; 95% CI: 1.22-6.94), red eyes (OR: 3.2; 95% CI: 1.5-6.8), voice loss (OR: 3.6; 95% CI: 1.6-
8.0), itchy eyes (OR: 2.2; 95% CI: 1.0-4.8) than other employees. When high levels of airborne NCl3 were taken into account
(airborne NCl3 levels ≥ 800 µg/m3
vs. < 800 µg/m3
) ocular and respiratory symptoms became much more evident, with higher
risks (as ORs) in exposed subjects (lifeguards and trainers) compared with other employees.
Conclusions: This study confirms that lifeguards and trainers are at risk for respiratory and ocular irritative symptoms more
than other employees in indoor swimming pools, in particular in presence of high airborne NCl3 levels.


Measuring halogenated disinfectants

CYA as a hypochlorous acid buffer

This post will describe the effects of using Cyanuric Acid (CYA) to lower active chlorine concentration in terms of breakpoint chlorination and the net resulting chloramine production. The basic breakpoint reaction was described by Griffin (1939), but the first reasonable detailed model was proposed by Wei & Morris (1974 — in Chapter 13 in the same “Chemistry of Water Supply, Treatment and Distribution” book that has the O’Brien paper on the chlorine/CYA equilibrium constants). Subsequent improvements were made to the model by Saunier & Selleck (1976) and most recently by Jafvert & Valentine (1992) and Vikesland, Ozekin and Valentine (2000) which should be considered to be the best model to-date. The following is the paper (a link to be able to purchase the most recent two online is here and here).

Chad T. Jafvert and Richard L. Valentine, “Reaction Scheme for the Chlorination of Ammoniacal Water”, Environ. Sci. Technol., Vol. 26, No. 3, 1992, pp. 577-585.

Though the model lists 14 reactions, including both forward and reverse reaction rates, the dominant reactions are the following:

(1) HOCl + NH3 —> NH2Cl + H2O
Hypochlorous Acid + Ammonia —> Monochloramine + Water

(2) HOCl + NH2Cl —> NHCl2 + H2O
Hypochlorous Acid + Monochloramine —> Dichloramine + Water

(3) HOCl + NHCl2 —> NCl3 + H2O
Hypochlorous Acid + Dichloramine —> Nitrogen Trichloride + Water

(4) NHCl2 + NCl3 + 2H2O —> 2HOCl + N2(g) + 3H+ + 3Cl
Dichloramine + Nitrogen Trichloride + Water —> Hypochlorous Acid + Nitrogen Gas + Hydrogen Ion + Chloride Ion

The first reaction producing monochloramine is by far the fastest. It is over 95% complete in one minute when the FC is around 10% of the CYA and the ammonia is much less than the chlorine so that the chlorine level remains fairly constant. With no CYA, the reaction is mostly complete in a couple of seconds. The subsequent reactions are far slower.

You can then see that hypochlorous acid participates in two reactions (after initially producing monochloramine quickly), one producing dichloramine and another producing nitrogen trichloride so the net reaction varies as the square of the hypochlorous acid concentration. You can see that nitrogen trichloride is broken down by dichloramine and the latter is produced with a reaction rate that varies linearly with hypochlorous acid concentration. So in the steady state, the amount of nitrogen trichloride is linearly dependent on the hypochlorous acid concentration. This can also be seen by the following rate reaction balance at steady state.

k3*[HOCl]*[NHCl2] = k4*[NHCl2]*[NCl3]
Rate of formation of Nitrogen Trichloride = Rate of destruction of Nitrogen Trichloride

so, k3*[HOCl] = k4*[NCl3]

The nitrogen trichloride concentration in the steady state is linearly proportional to the hypochlorous acid concentration. Since nitrogen trichloride is very volatile, this implies that the rate of outgassing of nitrogen trichloride may be proportional to the hypochlorous acid concentration since the outgassing rate is likely to be proportional to its concentration in the water.

A similar rate reaction balance for dichloramine gives the following.

k2*[HOCl]*[NH2Cl] = k3*[HOCl]*[NHCl2] + k4*[NHCl2]*[NCl3]
Rate of formation of Dichloramine = Rate of destruction of Dichloramine

and substituting the earlier steady-state equation we have

k2*[HOCl]*[NH2Cl] = k3*[HOCl]*[NHCl2] + k3*[HOCl]*[NHCl2]

which reduces to

k2*[NH2Cl] = 2*k3*[NHCl2]

So the ratio of monochloramine to dichloramine is constant and independent of hypochlorous acid concentration.

We can look at the steady-state for monochloramine assuming a constant introduction of ammonia into the water.

k1*[HOCl]*[NH3] = k2*[HOCl]*[NH2Cl]
Rate of formation of Monochloramine = Rate of destruction of Monochloramine

so the ratio of ammonia to monochloramine is constant and independent of hypochlorous acid concentration. Finally, we can look at the steady-state for ammonia.

k = k1*[HOCl]*[NH3]
Rate of formation of Ammonia = Rate of destruction of Ammonia

which says that for a constant rate of introduction of ammonia, the amount of ammonia, and therefore monochloramine and dichloramine (from above), are inversely proportional to the hypochlorous acid concentration.

Earlier models had reactions forming an intermediate, and the Jafvert & Valentine model has this as well, but it is not the dominant reaction in that model. The following shows the intermediate reactions such as found with Wei & Morris.

(5) NHCl2 + H2O —> NOH + 2H+ + 2Cl
Dichloramine + Water —> Intermediate + Hydrogen Ion + Chloride Ion

(6) NOH + NH2Cl —> N2(g) + H2O + H+ + Cl
Intermediate + Monochloramine —> Nitrogen Gas + Water + Hydrogen Ion + Chloride Ion

(7) NOH + NHCl2 —> N2(g) + HOCl + H+ + Cl
Intermediate + Dichloramine —> Nitrogen Gas + Hypochlorous Acid + Hydrogen Ion + Chloride Ion

In the Wei & Morris model, there is no destruction of nitrogen trichloride, so it’s rate of production is the product of the hypochlorous acid concentration and the dichloramine concentration. In the above, reaction (7) is more dominant than reaction (6). The formation of the intermediate NOH is a rate limiting step so dichloramine is built up and therefore the rate of production of nitrogen trichloride is linearly dependent on the hypochlorous acid concentration.

For a realistic example, consider a pool with 3 ppm FC and no CYA vs. a pool with 3 ppm FC and 30 ppm CYA. Both are at a pH of 7.5 (there is far more nitrogen trichloride produced at lower pH) and the temperature is 77F. If it is assumed that the chlorine level is maintained at a constant level and that there is a constant introduction of ammonia in the water at a rate of 0.1 ppm N per hour, then we have the following steady state amounts (using Jafvert & Valentine in a spreadsheet I made here):

SPECIES ……………………… NO CYA ………… 30 ppm CYA
Monochloramine …………. 0.02 ppm ……….. 0.70 ppm
Dichloramine ……………… 2.97 ppb ………… 85.42 ppb
Nitrogen Trichloride …….. 70.96 ppb ………. 2.35 ppb

You can see from the above that with no CYA in the water, there is less monochloramine and dichloramine but more nitrogen trichloride compared to having CYA in the water. The differences are roughly a factor of the CYA level because that is roughly the difference in the hypochlorous acid concentration (the breakpoint chlorination spreadsheet assumes 3 ppm FC with 30 ppm CYA results in about 0.05 ppm hypochlorous acid at pH 7.5 — the actual amount is closer to 0.042 ppm). Nitrogen trichloride is the most volatile and irritating. The monochloramine odor threshold is 0.65 ppm; for dichloramine it is 100 ppb; for nitrogen trichloride it is 20 ppb. The equilibrium concentrations in air for monochloramine and dichloramine are somewhat lower than that in water, but nitrogen trichloride is extremely volatile so will not saturate the air before becoming extremely noticeable and irritating.

The above is just for breakpoint chlorination of ammonia. As seen in Table 4.1 on document page 62 (PDF page 85) of this link, urea has 68% of the nitrogen in sweat compared to 18% for ammonia while in urine it’s 84% vs. 5%. There is no definitive model for oxidation of urea by chlorine, though some mechanisms have been proposed (by Wojtowicz) including the slow formation of a quad-chloro urea followed by rapid breakdown to dichloramine and nitrogen trichloride. If I repeat the above analysis using an 80%/20% split of urea to ammonia and assume a steady state buildup, then I get the following results.

SPECIES ……………………… NO CYA ………… 30 ppm CYA
Monochloramine …………. 0.01 ppm ……….. 0.28 ppm
Dichloramine ……………… 1.19 ppb ………… 34.17 ppb
Nitrogen Trichloride …….. 70.84 ppb ………. 2.35 ppb

You can see that the resulting nitrogen trichloride is the same as before, but that there is lower monochloramine and dichloramine by a factor of 2.5.

The rate of ammonia/urea introduction of 0.1 ppm N per hour is for heavy bather loads since it represents a chlorine usage of nearly 1 ppm FC per hour. One swimmer may produce around 0.1 ppm N per hour in 1000 gallons so only a pool with many people being active would have this sort of usage. Of course, having children in the water that urinate would provide a very high load. If a child urinates 100 ml (3.4 fluid ounces), then in 1000 gallons this is about 0.3 ppm N.

Note that the urea model assumes no interactions between the chloramines and chloroureas or related species and that’s probably not realistic, but there are no studies or models I can find analyzing such interactions.

Since the UV in sunlight breaks down nitrogen trichloride fairly quickly and since air circulation is also good outdoors, the current recommendations for FC as a % of CYA are reasonable for outdoor pools. The slower breakpoint is not generally a problem unless the bather load is high. For commercial/public pools with higher bather loads, an FC that is 20% of the CYA level may be more appropriate. For indoor pools, the slower breakpoint might be more of an issue so perhaps an FC that is 20% of the CYA level may be better even when there is not high bather load in such pools. From the models, not using any CYA at all in any pool (indoor or outdoor) can result in far higher irritating nitrogen trichloride concentrations and also has the chlorine level be too strong for corrosion and oxidizing swimsuits, skin and hair. Since it is not practical to maintain 0.2 ppm FC everywhere in an indoor pool due to local usage and imperfect circulation, using CYA as a hypochlorous acid buffer makes sense, but should not be overdone.

Pathways of trihalomethane uptake in swimming pools

Article: Pathways of trihalomethane uptake in swimming pools.
[hide abstract]
ABSTRACT: Chlorination of pool water leads to the formation of numerous disinfection by-products (DBPs), chloroform usually being most abundant. Bathers and pool guardians take up various amounts of DBPs by different pathways. Identification of different uptake paths is important in order to develop a technical strategy for swimming pool water treatment and to develop focussed technical solutions to minimize THM uptake. Basically, trihalomethanes (THMs) can be taken up by inhalation, by dermal absorption, or orally (swallowing of water). In our experimental study involving up to 17 participants we quantified the body burden resulting from exposure to three different concentrations of chloroform in water and air of an indoor swimming pool, during a 60 min exercising period. Chloroform concentration of the water was 20.7, 7.1, and 24.8 microg/l and was not influenced artificially. Corresponding air CHCl3 concentrations were measured at two different levels (20 cm and 150 cm) and ranged from to 85 to 235 microg/m3. To dissociate the dermal exposure route from that of inhalation, THM concentrations were measured in the blood of subjects practicing in an indoor pool with and without scuba tanks, as well as in the blood of subjects walking around the pool without swimming. Chloroform concentrations were measured in blood samples before and after each exercise period. Blood chloroform concentration of participants with scuba tanks was 0.32 +/- 0.26 microg/l, without scuba tanks 0.99 +/- 0.47 micro/l, and for persons walking around the pool 0.31 +/- 0.25 microg/l. Our results indicate that THMs are mainly taken up over the respiratory pathway. Only about one third of the total burden is taken up over the skin. We examined the relationship between blood concentration and environmental chloroform concentrations by using linear regression models. Blood concentrations are correlated to air chloroform concentrations; correlation to water concentrations is less obvious.

International Journal of Hygiene and Environmental Health 01/2005;

Optimizing Chloramine Treatment

Optimizing Chloramine Treatment

Nitrate Removal from Water

Treatment: Anion Exchange Water Softener (Countercurrent Regenerating)

image004A specialized type of Anion exchange water softener is used to remove nitrates. A water softener uses the principle of ion-exchange – in this case, anions – to remove nitrates from raw water. The equipment contains a “bed” of softening material known as ‘resin’ through which the untreated water flows. Although the anion softener looks the same on the outside, this unit is very different from a standard water softener. As water passes through the resin, the nitrates in the water attach themselves to this material. This ion-exchange process occurs literally billions of times during the softening process. Weekly automatic regeneration, or recharging, is necessary. The unit is set to automatically perform this regeneration as needed, based on water usage. To recharge the resin, it must be rinsed with a rich brine solution (Sodium Chloride – salt). This washes the nitrates out of the resin and replaces them with chloride, so the resin is once again ready to exchange ions to remove more nitrates. During the recharging cycle, the unit is also backwashed. Reversing the normal flow of water also serves to remove any turbidity and sediment, which may have accumulated during the softening process due to the filtering action of the ion exchange material.  Backwashing also loosens and fluffs up the bed of resin. Countercurrent regenerating water softeners add the salt against the service flow, and use significantly less salt than traditional water softeners. Our softeners are controlled using Clack® WS-1 control heads, which offer the option of either metered “demand initiated regeneration” or the more traditional “timed” regeneration.

Chloramine toxicity

Chloramine toxicity.

“Chlorine is an oxidizer, which burns a fishes’ gills. Chloramines, on the other hand, pass across the gills of a fish and into its blood, where the molecule attaches to the hemoglobin, acting like nitrite to induce methemoglobinemia. The toxicity of chloramines is affected by pH, I’m reading at FishDoc, with Chloramine-T more toxic at lower pH. Fish stricken by chloramine poisoning are sluggish and respire heavily.”

And we thought it was from over-training!?