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Partial Pressure

Partial pressure

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In a mixture of ideal gases, each gas has a partial pressure which is the pressure which the gas would have if it alone occupied the volume.[1] The total pressure of a gas mixture is the sum of the partial pressures of each individual gas in the mixture.

In chemistry, the partial pressure of a gas in a mixture of gases is defined as above. The partial pressure of a gas dissolved in a liquid is the partial pressure of that gas which would be generated in a gas phase in equilibrium with the liquid at the same temperature. The partial pressure of a gas is a measure of thermodynamic activity of the gas’s molecules. Gases will always flow from a region of higher partial pressure to one of lower pressure; the larger this difference, the faster the flow. Gases dissolve, diffuse, and react according to their partial pressures, and not necessarily according to their concentrations in a gas mixture.




[edit] Dalton’s law of partial pressures

Main article: Dalton’s law

The partial pressure of an ideal gas in a mixture is equal to the pressure it would exert if it occupied the same volume alone at the same temperature. This is because ideal gas molecules are so far apart that they don’t interfere with each other at all. Actual real-world gases come very close to this ideal.

A consequence of this is that the total pressure of a mixture of ideal gases is equal to the sum of the partial pressures of the individual gases in the mixture as stated by Dalton’s law.[2] For example, given an ideal gas mixture of nitrogen (N2), hydrogen (H2) and ammonia (NH3):

P = P_{{\mathrm{N}}_2} + P_{{\mathrm{H}}_2} + P_{{\mathrm{NH}}_3}
P \, = total pressure of the gas mixture
P_{{\mathrm{N}}_2} = partial pressure of nitrogen (N2)
P_{{\mathrm{H}}_2} = partial pressure of hydrogen (H2)
P_{{\mathrm{NH}}_3} = partial pressure of ammonia (NH3)

[edit] Ideal gas mixtures

The mole fraction of an individual gas component in an ideal gas mixture can be expressed in terms of the component’s partial pressure or the moles of the component:

x_{\mathrm{i}} = \frac{P_{\mathrm{i}}}{P} = \frac{n_{\mathrm{i}}}{n}

and the partial pressure of an individual gas component in an ideal gas can be obtained using this expression:

P_{\mathrm{i}} = x_{\mathrm{i}} \cdot P
xi = mole fraction of any individual gas component in a gas mixture
Pi = partial pressure of any individual gas component in a gas mixture
ni = moles of any individual gas component in a gas mixture
n = total moles of the gas mixture
P = total pressure of the gas mixture

The mole fraction of a gas component in a gas mixture is equal to the volumetric fraction of that component in a gas mixture.[3]

[edit] Vapor pressure

Main article: Vapor pressure

A typical vapor pressure chart for various liquids

Vapor pressure is the pressure of a vapor in equilibrium with its non-vapor phases (i.e., liquid or solid). Most often the term is used to describe a liquid‘s tendency to evaporate. It is a measure of the tendency of molecules and atoms to escape from a liquid or a solid. A liquid’s atmospheric pressure boiling point corresponds to the temperature at which its vapor pressure is equal to the surrounding atmospheric pressure and it is often called the normal boiling point.

The higher the vapor pressure of a liquid at a given temperature, the lower the normal boiling point of the liquid.

The vapor pressure chart to the right has graphs of the vapor pressures versus temperatures for a variety of liquids.[4] As can be seen in the chart, the liquids with the highest vapor pressures have the lowest normal boiling points.

For example, at any given temperature, propane has the highest vapor pressure of any of the liquids in the chart. It also has the lowest normal boiling point(-43.7 °C), which is where the vapor pressure curve of propane (the purple line) intersects the horizontal pressure line of one atmosphere (atm) of absolute vapor pressure.

[edit] Equilibrium constants of reactions involving gas mixtures

It is possible to work out the equilibrium constant for a chemical reaction involving a mixture of gases given the partial pressure of each gas and the overall reaction formula. For a reversible reaction involving gas reactants and gas products, such as:

a\,A + b\,B \leftrightarrow c\,C + d\,D

the equilibrium constant of the reaction would be:

K_P = \frac{P_C^c\, P_D^d} {P_A^a\, P_B^b}
KP =  the equilibrium constant of the reaction
a =  coefficient of reactant A
b =  coefficient of reactant B
c =  coefficient of product C
d =  coefficient of product D
P_C^c =  the partial pressure of C raised to the power of c
P_D^d =  the partial pressure of D raised to the power of d
P_A^a =  the partial pressure of A raised to the power of a
P_B^b =  the partial pressure of B raised to the power of b

For reversible reactions, changes in the total pressure, temperature or reactant concentrations will shift the equilibrium so as to favor either the right or left side of the reaction in accordance with Le Chatelier’s Principle. However, the reaction kinetics may either oppose or enhance the equilibrium shift. In some cases, the reaction kinetics may be the over-riding factor to consider.

[edit] Henry’s Law and the solubility of gases

Main article: Henry’s Law

Gases will dissolve in liquids to an extent that is determined by the equilibrium between the undissolved gas and the gas that has dissolved in the liquid (called the solvent).[5] The equilibrium constant for that equilibrium is:

(1)     k = \frac {P_X}{C_X}
k =  the equilibrium constant for the solvation process
PX =  partial pressure of gas X in equilibrium with a solution containing some of the gas
CX =  the concentration of gas X in the liquid solution

The form of the equilibrium constant shows that the concentration of a solute gas in a solution is directly proportional to the partial pressure of that gas above the solution. This statement is known as Henry’s Law and the equilibrium constant k is quite often referred to as the Henry’s Law constant.[5][6][7]

Henry’s Law is sometimes written as:[8]

(2)     k' = \frac {C_X}{P_X}

where k‘ is also referred to as the Henry’s Law constant.[8] As can be seen by comparing equations (1) and (2) above, k‘ is the reciprocal of k. Since both may be referred to as the Henry’s Law constant, readers of the technical literature must be quite careful to note which version of the Henry’s Law equation is being used.

Henry’s Law is an approximation that only applies for dilute, ideal solutions and for solutions where the liquid solvent does not react chemically with the gas being dissolved.

[edit] Partial pressure in diving breathing gases

In recreational diving and professional diving the richness of individual component gases of breathing gases is expressed by partial pressure.

Using diving terms, partial pressure is calculated as:

partial pressure = total absolute pressure x volume fraction of gas component

For the component gas “i”:

ppi = P x Fi

For example, at 50 metres (165 feet), the total absolute pressure is 6 bar (600 kPa) (i.e., 1 bar of atmospheric pressure + 5 bar of water pressure) and the partial pressures of the main components of air, oxygen 21% by volume and nitrogen 79% by volume are:

ppN2 = 6 bar x 0.79 = 4.7 bar absolute
ppO2 = 6 bar x 0.21 = 1.3 bar absolute
ppi = partial pressure of gas component i  = Pi in the terms used in this article
P = total pressure = P in the terms used in this article
Fi = volume fraction of gas component i  =  mole fraction, xi, in the terms used in this article
ppN2 = partial pressure of nitrogen  = P_{{\mathrm{N}}_2} in the terms used in this article
ppO2 = partial pressure of oxygen  = P_{{\mathrm{O}}_2} in the terms used in this article

The minimum safe lower limit for the partial pressures of oxygen in a gas mixture is 0.16 bar (16 kPa) absolute. Hypoxia and sudden unconsciousness becomes a problem with an oxygen partial pressure of less than 0.16 bar absolute. Oxygen toxicity, involving convulsions, becomes a problem when oxygen partial pressure is too high. The NOAA Diving Manual recommends a maximum single exposure of 45 minutes at 1.6 bar absolute, of 120 minutes at 1.5 bar absolute, of 150 minutes at 1.4 bar absolute, of 180 minutes at 1.3 bar absolute and of 210 minutes at 1.2 bar absolute. Oxygen toxicity becomes a risk when these oxygen partial pressures and exposures are exceeded. The partial pressure of oxygen determines the maximum operating depth of a gas mixture.

Nitrogen narcosis is a problem when breathing gases at high pressure. Typically, the maximum total partial pressure of narcotic gases used when planning for technical diving is 4.5 bar absolute, based on an equivalent narcotic depth of 35 metres (110 ft).

With the acceptance of ASHRAE (American Society of Heating, Refrigerating
and Air-Conditioning Engineers) Code 62 concerning indoor air quality, more
stringent reviews are required of an indoor pool’s air quality. This technical bulletin
summarizes the chemistry involved for pool water using chlorine and its effects
on air quality, and vice versa. It also reviews the impact of ventilation air on air
quality, as well as the use of special filters to remove airborne contaminants in
a pool facility.
Many detailed articles are available about this subject from other sources. This
bulletin summarizes only the basics about pool chemistry to provide an
overview. Contact the NSPI (National Spa and Pool Institute) for more information.
Chlorine is added to water to form hypochlorous acid (HClO), an excellent
bactericide. In this solution it is known as “free chlorine,” and is highly reactive.
The free chlorine reacts with organic wastes introduced into the pool water –
such as sweat, urine, perfumes and other ammonia-based impurities – to form
new “combined chlorine” compounds. These new compounds have very poor
bactericide properties. If enough free chlorine is present, it reacts with the
combined chlorine compounds to further break them down into basic
elements, such as H2O (water), CO2 (carbon dioxide gas), N2 (nitrogen gas)
and various salts. When this breakdown process occurs, the pool is deemed to
be safe for swimmers.
Whether or not the complete breakdown can occur, however,
is a function of the amount of free chlorine available as
compared to the amount of ammonia-containing wastes present.
Table 1 summarizes the pool conditions resulting from various
ratios of free chlorine to chlorine compounds.
Technical Bulletin 9
Figure 2 – Outdoor air changes equilibrium point.
(lower CL•A concentration yields higher ratio)
Figure 3 – Outdoor air and chlorine removal filters significantly
change equilibrium point for highest ratio.
Figure 1 – Pool facility at equilibrium.
(Note: CL•A = chloramine concentration)
Table 1
Ratio Compound Present Comments
<5:1 Mono-chloramines Quick reaction; very poor disinfecting capacity (100x less)
5:1 to 10:1 Di-chloramines “Chlorine” odor; poor disinfecting capacity
>10:1 Basic elements Properly treated pool
As Table 1 shows, a constant source of free chlorine is needed
to ensure the complete reaction. This is known as breakpoint
chlorination. If the combined chlorine compounds are not
eliminated, pool “shocking” is required: a larger dose of chlorine
is added to the water to complete the reaction and balance the pool.
118 10/06
The pool room odor commonly described as “chlorine”
(which, in fact, is the odor produced by chloramine compounds),
occurs when the pool water chemistry is improperly balanced.
The chloramines readily release into the air and reach a balance
based on a chemical law known as the partial pressure
law. In laymen’s terms, this law states how much chloramine
remains in the water and how much is released to the air
under various conditions.
The ASHRAE 62 ventilation code recognizes this “chlorine” smell
as a potential indoor air quality problem and offers specific
recommendations for the introduction of outdoor air based
on the size of the pool and deck. (Refer to Desert Aire’s
Technical Bulletin 5 – Ventilation Air for Indoor Pools, for
details on these recommendations.) The code attempts to
replace the indoor air once per hour to eliminate the odor.
Since nature requires a balance, removing some of the
chloramines from the air will cause more chloramines to be
released from the water. Table 1 shows that the release of more
chloramines to the air will improve the free chlorine ratio,
bringing the pool chemistry a step closer to proper balance.
The response of some pool designers is to go beyond
ASHRAE 62 air quality recommendations. That scenario,
however, can introduce other problems.
First, in cold climates, wintertime outdoor air must be heated.
For even the smallest pools, this adds up to thousands of dollars
per month in increased utility bills.
Second, the code requires that relative indoor humidity
remain below 60 percent. Summer conditions in most locales
add humidity to the space, so when an increased air volume
is introduced, the facility may no longer be compliant with the
indoor humidity code.
While this technical bulletin does not attempt to cover all
chemistry issues (for example, the influence of pH on free
chlorine), it does demonstrate the basic chemical interaction
occurring in an indoor pool facility.
The following design specifications are recommended:
1. Automatic chlorate control system. The chemical feed
pump must be sized to match worst case pool loading.
2. High water turnover to better mix the pool, to avoid
dead spots, and to provide better chlorine concentration
measurement and control.
3. Ensure ASHRAE 62 outdoor air compliance to aid in
breakpoint chlorination.
4. Add chlorine deactivating filters to help balance
energy, humidity and water chemistry demands.
Adding special chlorine deactivating filters to the pool room
results in additional chloramine removal, thereby decreasing
the amount of free chlorine required to reach breakpoint
chlorination. Using these types of filters in lieu of bringing in
more outdoor air avoids temperature and humidity problems
and treatment expense in a pool facility.
Chlorine deactivating filters are added to the dehumidification
air handler as an alternative to standard disposable filters.
Interaction of Pool Water and Air Chemistry
N120 W18485 Freistadt Road
Germantown, WI 53022
PH: (262) 946-7400
FAX: (262) 946-7401

Chloroform Detection and Quantification

2.3  Conversion factors

         1 mg chloroform/m3 air = 0.204 ppm at 25 °C and 101.3 kPa
         (760 mmHg)

         1 ppm = 4.9 mg chloroform/m3 air

    2.4  Analytical methods

         Many analytical methods for the determination of chloroform
    residues in air, water and biological samples have been reported.
    Table 2 summarizes some of the procedures used in the literature for
    sampling and determining chloroform in different media. The
    detection limits are included in Table 2. Although all of these
    methods were developed to detect chloroform at very low levels, some
    of them can be used only in cases where chloroform is present at
    relatively high levels.

         Since chloroform is very volatile, care must be taken while
    sampling and handling samples to prevent any chloroform from being
    lost during such procedures. In this case, accuracy depends very
    much on the repeatability of the method being used. All but one of
    the methods given in Table 2 use gas chromatographic techniques with
    electron capture detection (ECD), flame ionisation detection (FID),
    photo-ionisation detection (PID) or mass spectrometry (MS) for

        Table 2.  Sampling and analysis of chloroform
    Medium    Sample method               Analytical method   Detection limit   Sample size     Comments                      Reference

    Air       aspiration velocity of      MIRAN-infrared      300 µg/m3                         can be used only when         Lioy & Lioy
              28 litres/min, trajectory   spectrometer                                          CHCl3 is presented at         (1983)
              of 20 m                                                                           high levels

    Air       direct injection            GC with a           0.5 µg/m3         5 ml injected   method involves the use of    Lasa et al.
                                          coulometric ECD                                       a continuously operating      (1979)
                                                                                                automatic GC monitor

    Air       direct injection,           GC with two         > 0.4 µg/m3       8 ml injected   efficiency followed from      Lillian &
              calibration gas used for    ECDs installed      (estimated)                       signal ratios of the          Singh (1974)
              reliability                 serially                                              two ECDs

    Air       AIRSCAN/PHOTOVAC            GC-PID              0.5 µg/m3         0.05-1 ml       portable machine, suitable    Leveson et
              direct injection                                                                  for field monitoring          al. (1981)

    Air       adsorption on activated     GC-ECD              approximately     1 m3/24 h       in 1984 the draft standard    NNI (1984)
              charcoal, desorption                            0.1 µg/m3                         NVN 2794 needed to be
              with CS2                                                                          tested for usefulness

    Air       adsorption on Porapak-N,    GC-ECD              1 µg/m3           20 litres       advantage of methanol is the  Van Tassel et
              desorption with 1-2 ml                                                            absence of a background       al. (1981)
              methanol                                                                          signal in the ECD

    Air       adsorption on Porapak-N,    GC-ECD              estimated to      0.3-3 litres    confirmation of results by    Russell &
              thermal desorption at                           be 0.05 µg/m3                     use of GC-MS                  Shadoff (1977)
              200 °C

    Air       adsorption on               GC-ECD-FID two      approximately     1-3 litres                                    Heil et al.
              Chromosorb-102, thermal     detectors           0.06 µg/m3                                                      (1979)
              desorption at 150 °C        positioned in


    Table 2 (contd)
    Medium    Sample method               Analytical method   Detection limit   Sample size     Comments                      Reference

    Air       adsorption on Tenax,        GC-FID              0.08 µg/m3        2 ml injected                                 Kebbekus &
              sample rate 10-15 ml/min,   GC-MS                                                                               Bozzelli (1982)
              thermal desorption and

    Air       adsorption on Tenax-GC,     GC-MS               0.2 µg/m3         20 litres                                     Krost et al.
              cooled with liquid                                                                                              (1982)
              nitrogen, thermal
              desorption at 270 °C

    Air       adsorption on activated     GC-FID with         0.15 mg           up to 30        these two types of detection  Morele et
              coal, desorption with       TCEP,               detector          litres can be   appeared to complement        al. (1989)
              CS2, using                  Chromosorbsen       sitivity          sampled         each other
              methylcyclohexane as IS     column

              adsorption on activated     GC-ECD with 5%      2 µg is 
              coal, desorption with       CV17, Chromosorb    minimum 
              ethanol, using              column              quantifiable 
              trichloroethylene as IS                         value

    Air       collection on charcoal,     GC-FID              0.01 mg per       up to 15        suitable for simultaneous     US NIOSH
              desorption with CS2 using                       sample            litres can be   analysis of two or more       (1984)
              n-undecane as IS                                estimated         sampled         substances

    Air       cold trap, heating the      GC-ECD              0.01 µg/m3        30 ml in        air samples were taken        Harsch &
              cold trap                                                         cold trap       in the stratosphere           Cronn (1978)

    Air       injection into cold trap,   GC-MS (SIM)         0.03 µg/m3        100 ml in                                     Cronn &
              heating the cold trap                                             cold trap                                     Harsch (1979)


    Table 2 (contd)
    Medium    Sample method               Analytical method   Detection limit   Sample size     Comments                      Reference

    Air       cold trap after desication  GC-PID-ECD-FID,     0.005 µg/m3       1 litre         during the process the        Rudolph &
              with magnesium              3 detectors                                           column is kept at -103 °C     Jebsen (1983)
              perchlorate, heating the    placed                                                (cryofocusing)
              cold trap to 257 °C         sequentially

    Breath    collection on Tenax GC      GC-MS               0.11 µg/m3                        suitable for quantitative     Pellizzari
              cartridge, thermal                                                                analysis, one sample in       et al.
              desorption                                                                        1.5 h                         (1985b)

    Water     headspace, CH2Br2 was       headspace GC-ECD    0.02 µg/litre     500 µl          suitable for routine          Herzfeld et
              used as IS                                                        injected        analysis over a wide range    al. (1989)
                                                                                                of differently composed 
                                                                                                river waters

    Water     pentane extraction          GC-ECD using        1 µg/litre        100 ml          suitable for routine          Oliver (1983)
                                          2 mm x 4 mm i.d.                      extracted with  measurements in 
                                          column backed with                    10 ml pentane,  drinking-water
                                          Squalane on                           24 litres of
                                          Chromosorb P                          extract used
                                                                                for injection

    Water     liquid-liquid extraction    GC with a Hall      0.10 µg/litre     3 µl injected   suitable for routine          Mehran et al.
              with pentane                electrolyte                                           analyses                      (1984)
                                          Tenax-GC column

    Water     direct aqueous injection    GC-ECD with a       0.02 µg/litre     2 µl injected   suitable for analyses of      Grob (1984)
              of sample into GC           fused silica                                          halocarbons in the 0.01-10
                                          capillary column                                      ppb range


    Table 2 (contd)
    Medium    Sample method               Analytical method   Detection limit   Sample size     Comments                      Reference

    Water     direct aqueous injection    GC-ECD with a       0.1 µl/litre      1 µl injected   easy, fast and reliable       Temmerman &
              of sample into GC           methyl-silicone                                       technique for everyday        Quaghebeur
                                          fused silica                                          quality control               (1990)
                                                                                                capillary column

    Aqueous   diethyl ether extraction    GC-MS with a        < 1 µg/litre      200 ml          suitable for water and        Meier et al.
              with 25 µg                  fused silica        and recovery      extracted,      homogenized environmental     (1985)
              p-bromofluorobenzene        capillary column    efficiency of     extract         samples
              as IS                                           0.85              concentrated
                                                                                to 1 ml, 2 µl

    Blood     headspace, magnesium        headspace           0.0225 µg/litre   200 µl          suitable for direct           Aggazzotti
              sulfate heptahydrate and    GC-ECD, with        (2.5 times        injected        measurements of CHCl3         et al.
              n-octyl alcohol were        Chromosorb          standard                                                        (1987)
              added to the plasma         W AW column         deviation)

    Blood     passing inert gas over      GC-MS               3 µg/litre        1-10 ml         suitable for quantitative     Pellizzari
              warmed blood sample,                                                              analysis of CHCl3 in          et al.
              collection on Tenax-GC,                                                           blood                         (1985a)
              thermal desorption

    Blood     diethyl ether extraction    GC-MS with a        qualitative (no   1-5 ml,         suitable for identification   Mink et al.
    plasma    (1:1) with 3 different      fused silica        detection limit   extract         of CHCl3 in biological        (1983)
    and       internal standards added    capillary column    was given)        concentrated    samples
    stomach   to the concentrated                                               to 1 ml of
    contents  extract                                                           of which 2µl
                                                                                is injected


    Table 2 (contd)
    Medium    Sample method               Analytical method   Detection limit   Sample size     Comments                      Reference

    Tissue    maceration in water,        GC-MS               6 µg/kg           5 g             suitable for semi-            Pellizzari
              collection on Tenax-GC,                                                           quantitative analysis of      et al.
              thermal desorption                                                                chloroform in tissues         (1985a)

    Urine     pentane extraction          GC-ECD              < 1 µg/litre      2 µl of         convenient and sensitive      Youssefi
                                                                                extract         means for determining         et al.
                                                                                injected        light halogenated             (1978)

    Fish      extraction with pentane     GC-ECD with a       1 µg/kg in        2 µl            extraction efficiency of      Baumann
              and isopropanol,            fused silica        fresh             injected        67%                           Ofstad et
              bromotrichloromethane       capillary column    material                                                        al. (1981)
              used as IS



       ECD = electron capture detector; FID = flame ionisation detector; GC = gas chromatography; IS = internal standard;
       MS = mass spectrometry; PID = photo-ionisation detector; SIM = selected ion monitoring

    measuring chloroform residues. Only the first method listed depends
    on the use of a MIRAN-infrared spectrometer. The sensitivity of this
    method is very poor.

    2.4.1  Sampling and analysis in air

         The methods reported in Table 2 for sampling and analysis of
    chloroform levels in air can be grouped into four different
    categories.  Direct measurement

         In this type of procedure, air is aspirated or injected
    directly into the measuring instrument without pretreatment.
    Although these methods are simple, they can be used only when
    chloroform is present in the air at relatively high levels (e.g.,
    urban source areas, see section 5.1.1).  Adsorption-liquid desorption

         Air samples analysed for their chloroform levels are conducted
    through an activated adsorbing agent (e.g., charcoal or Porapak-N).
    The adsorbed chloroform is then desorbed with an appropriate solvent
    (e.g., carbon disulfide or methanol) and subsequently passed through
    the gas chromatograph (GC) for measurement.  Adsorption-thermal desorption

         In this technique, air samples are also passed through an
    activated absorbing agent (e.g., Tenax-GC, Porapak-Q, Porapak-N or
    carbon molecular sieve). The adsorbed chloroform is then thermally
    desorbed and driven into the GC column for determination.  Cold trap-heating

         In this type of procedure, air samples are injected into a cold
    trap (liquid nitrogen or liquid oxygen are used for cooling). The
    trap is then heated while transferring its chloroform content into
    the packed column of a GC for measurement.

    2.4.2  Sampling and analysis in water

         Several methods of sampling and analysing water for chloroform
    content are included in Table 2. In some of these methods, water
    samples are directly injected into a wide bore or fused silica
    capillary column to which an ECD is attached. In some other water
    analysis procedures mentioned in Table 2, the chloroform in the
    water samples is first extracted by means of a non-polar,
    non-halogenated solvent (e.g.,  n-pentane). Samples of the obtained
    extracts are then injected into the GC for determining chloroform.

    In another procedure, referred to as "close-loop-stripping analysis"
    (CLSA), chloroform is removed from the water sample by purging it
    with a large volume of a gas (e.g., nitrogen); the gas is then
    passed through an adsorption tube and subsequently analysed by
    GC-MS. Using this latter method, a million-fold concentration can be
    achieved, so that chloroform can be quantified even at very low
    levels. A headspace GC technique with ECD has also been used for
    measuring chloroform levels in water samples (see Table 2).

    2.4.3  Sampling and analysis in biological samples  Blood and tissues

         Several procedures for determining chloroform in blood and
    tissue samples are presented in Table 2. A headspace GC technique
    has been used for direct measurement of chloroform in plasma
    obtained from subjects exposed to low levels in air (Aggazzotti et
    al., 1987). The second procedure (Kroneld, 1985) depends on
    liquid-liquid extraction of chloroform from blood samples and
    subsequent injection of the extract into a GC system for
    quantification. In the method of Pellizzari et al. (1985a),
    chloroform is evaporated by passing an inert gas over a warmed
    plasma or macerated tissue sample with adsorption of the vapour on a
    Tenax GC column, and is then recovered by thermal desorption and
    analysed by GC-MS.  Urine

         Youssefi et al. (1978) measured chloroform concentration in
    urine using pentane extraction and GC-ECD analysis.

DBP N-nitrosodimethyamine, haloacetonitriles, haloacetaldehydes

Environ Sci Technol. 2009 Nov 1;43 (21):8320-8325 19924963 (P,S,G,E,B,D)
Water Quality Laboratory, Metropolitan Water District of Southern California, 700 Moreno Avenue, La Verne, California 91750, Department of Civil, Environmental and Sustainable Engineering, Engineering Center (G-Wing), Arizona State University, Room ECG-252, Tempe, Arizona 85287-5306, Center for Environmental Biotechnology, Biodesign Institute, Arizona State University, P.O. Box 875701, Tempe, Arizona 85287-5701, and King Abdullah University of Science and Technology, Box 55455, Jeddah, 21534, Saudi Arabia.
Effluents from wastewater treatment plants (WWTPs) contain disinfection byproducts (DBPs) of health concern when the water is utilized downstream as a potable water supply. The pattern of DBP formation was strongly affected by whether or not the WWTP achieved good nitrification. Chlorine addition to poorly nitrified effluents formed low levels of halogenated DBPs, except for (in some cases) dihalogenated acetic acids, but often substantial amounts of N-nitrosodimethyamine (NDMA). Chlorination of well-nitrified effluent typically resulted in substantial formation of halogenated DBPs but much less NDMA. For example, on a median basis after chlorine addition, the well-nitrified effluents had 57 mug/L of trihalomethanes [THMs] and 3 ng/L of NDMA, while the poorly nitrified effluents had 2 mug/L of THMs and 11 ng/L of NDMA. DBPs with amino acid precursors (haloacetonitriles, haloacetaldehydes) formed at substantial levels after chlorination of well-nitrified effluent. The formation of halogenated DBPs but not that of NDMA correlated with the formation of THMs in WWTP effluents disinfected with free chlorine. However, THM formation did not correlate with the formation of other DBPs in effluents disinfected with chloramines. Because of the relatively high levels of bromide in treated wastewater, bromine incorporation was observed in various classes of DBPs.


Water Testing 101: TDS

Terms & Conditions of Use

An overview of the most common parameter for testing water quality

– By Rob Samborn

Of all the buzzwords that are swimming around the world of water quality these days, “TDS” is one of the most common. Industry professionals range from being fully versed in the subject to being marginally aware, while the average consumer would most likely guess it is an abbreviation for touchdowns. Given that TDS is by far the most common parameter for water quality testing, an overview of the subject is warranted.

According to Wikipedia, total dissolved solids (TDS) is defined as “the combined content of all inorganic and organic substances contained in a liquid that are present in a molecular, ionized or microgranular suspended form.” The article goes on to state that “total dissolved solids are differentiated from total suspended solids (TSS) in that the latter cannot pass through a sieve of two micrometers but are indefinitely suspended in solution.”

In other words, TDS is anything—other than the pure H2O—in water that you cannot see. This could include any salt, metal or mineral, and the lower the TDS level is, the purer the water.

So then why should TDS be measured? As an overall indicator of water purity, TDS is an especially important parameter, and more often than not, it is the first one tested. A TDS test is quick, easy and inexpensive. A single TDS meter can be used thousands of times, requiring nothing more than the occasional recalibration and new batteries.

Water filtration, treatment and purification often become a question of cost-effectiveness. Knowing the TDS level will help determine what, if any, type of system or process is required. Along these lines, a TDS meter is an excellent tool for determining the efficacy of many types of water filtration and purification systems.

Many people still rely on the old-fashioned methods of time or flow to determine when the filter cartridge or membrane needs to be changed. Because usage may vary and the TDS levels of water supplies fluctuate, time and flow are far from precise methods. With improved technology in TDS measurement being coupled with accessible prices, the focus is definitely moving away from a reliance on time and flow.

How is TDS Measured?

TDS is measured on a quantity scale, either in mg/L or, more commonly, in parts per million (ppm). Simply put, if the TDS level is 335 ppm, this means that out of one-million parts of H2O, 335 of those parts are something else.

The only true method of measuring TDS is to evaporate a water sample and weigh the remains with a precision analytical balance. While this is the most reliable and accurate method, it is also costly. Because a precision analytical balance that can evaporate water is not on the top of the average water industry professional’s shopping list, there are alternatives. Over the past few decades, companies have developed TDS meters—inexpensive tools to help measure TDS in water.

Ironically, a TDS meter does not initially measure TDS, which is where much of the confusion arises. TDS meters, also known as TDS testers or indicators, are digital or analog meters that measure the electrical conductivity of water. Based on that conductivity, the meters estimate what the true TDS level might be.

As stated previously, TDS is essentially anything dissolved in the water other than the pure H2O. Because hydrogen and oxygen conduct virtually no electricity, and most other elements do, the conductivity measurement is a fair indicator of the overall water purity.

In reality, a TDS meter measures the electrical conductivity of water or, in other words, the total amount of mobile charged ions found in water. If an element is dissolved in water and can conduct electricity, it is called an electrolyte. Salt, for example, is an electrolyte. Sugar, however, is not and will therefore not register on a conductivity or TDS meter. This is one reason why a TDS meter is only an estimate of the true TDS.

Additionally, different types of water will contain different quantities of certain dissolved substances. For example, seawater will naturally have far more salt than freshwater. To accommodate this difference, TDS meters will incorporate conversion factors, typically ranging from 0.4 to 1, to convert the conductivity to the estimated TDS level. As a general rule of thumb, the higher the conductivity, the higher the conversion factor.

Although the measurement on a TDS meter is an estimate, it is reasonably accurate. When simplicity, accessibility and cost are taken into account compared with a precision analytical balance, a TDS meter is more than sufficient for most applications.

A common question that arises is: “At what TDS level should tap water be?” There is no right or wrong answer to this question because the TDS levels of tap water fluctuate widely from location to location and from day to day. Pipe age can affect TDS levels, as can precipitation (or lack thereof).

Neither the U.S. federal government nor any of the states set minimum TDS levels on water; however, maximum levels are set. Some of these levels are enforceable, while others are only recommendations. The U.S. Environmental Protection Agency includes TDS on its list of National Secondary Drinking Water Regulations (NSDWR) and sets a limit of 500 mg/L; however, the NSDWRs are nonenforceable guidelines.

What Else does TDS Affect?

Besides drinking water, TDS affects anything that consumes, lives in or uses water. For example, high levels of TDS will result in excessive scaling in pipes. On the other hand, low levels of TDS may be unhealthy for plants and fish.

The measurement of TDS in water is also extremely important for certain pharmaceutical, manufacturing, industrial, medical and agricultural applications, to name a few.

With a number of economically priced, accurate and easy-to-use TDS meters available on the market, there is no reason not to use one.

Water Deionizers, Deionization Solutions


Pure Aqua is a leading provider of deionization solutions. Our water deionizers are rugged, pre-engineered, pre-assembled, standardized units that minimize expensive installation and start-up costs. We have designed our Deionization systems to maximize the efficiency and repeatability of the unit during the service and regeneration modes

The Process of Deionization or Ion-exchange

In the context of water purification, ion-exchange is a rapid and reversible process in which impurity ions present in the water are replaced by ions released by an ion-exchange resin. The impurity ions are taken up by the resin, which must be periodically regenerated to restore it to the original ionic form. (An ion is an atom or group of atoms with an electric charge. Positively-charged ions are called cations and are usually metals; negatively-charged ions are called anions and are usually non-metals).

The following ions are widely found in raw waters:

Cations Anions
Calcium (Ca2+) Chloride (Cl)
Magnesium (Mg2+) Bicarbonate (HCO3)
Sodium (Na+) Nitrate (NO3)
Potassium (K+) Carbonate (CO32-)
Iron (Fe2+) Sulfate (SO42-)

Ion Exchange Resins

There are two basic types of resin – cation-exchange and anion-exchange resins. Cation exchange resins will release Hydrogen (H+) ions or other positively charged ions in exchange for impurity cations present in the water. Anion exchange resins will release hydroxyl (OH) ions or other negatively charged ions in exchange for impurity anions present in the water.

The application of ion-exchange to water treatment and purification

There are three ways in which ion-exchange technology can be used in water treatment and purification: first, cation-exchange resins alone can be employed to soften water by base exchange; secondly, anion-exchange resins alone can be used for organic scavenging or nitrate removal; and thirdly, combinations of cation-exchange and anion-exchange resins can be used to remove virtually all the ionic impurities present in the feedwater, a process known as deionization. Water deionizers purification process results in water of exceptionally high quality.


For many laboratory and industrial applications, high-purity water which is essentially free from ionic contaminants is required. Water of this quality can be produced by deionization.The two most common types of deionization are:

  • Two-bed deionization
  • Mixed-bed deionization

Two-bed deionization

The two-bed deionizer consists of two vessels – one containing a cation-exchange resin in the hydrogen (H+) form and the other containing an anion resin in the hydroxyl (OH) form. Water flows through the cation column, whereupon all the cations are exchanged for hydrogen ions.To keep the water electrically balanced, for every monovalent cation, e.g. Na+, one hydrogen ion is exchanged and for every divalent cation, e.g. Ca2+, or Mg2+, two hydrogen ions are exchanged. The same principle applies when considering anion-exchange. The decationised water then flows through the anion column. This time, all the negatively charged ions are exchanged for hydroxide ions which then combine with the hydrogen ions to form water (H2O).

Mixed-bed deionization

In mixed-bed deionizers the cation-exchange and anion-exchange resins are intimately mixed and contained in a single pressure vessel. The thorough mixture of cation-exchangers and anion-exchangers in a single column makes a mixed-bed deionizer equivalent to a lengthy series of two-bed plants. As a result, the water quality obtained from a mixed-bed deionizer is appreciably higher than that produced by a two-bed plant.

Although more efficient in purifying the incoming feedwater, mixed-bed plants are more sensitive to impurities in the water supply and involve a more complicated regeneration process. Mixed-bed deionizers are normally used to ‘polish’ the water to higher levels of purity after it has been initially treated by either a two-bed deionizer or a reverse osmosis unit.


EDI Electrodeionization Systems remove ions from aqueous streams, typically in conjunction with reverse osmosis (RO) and other purification devices. Our high-quality deionization modules continually produce ultrapure water up to 18.2MW/cm. EDI may be run continuously or intermittently

Chlorine and Health

from Intec-America

Chlorine and Health

In recent years, there have been numerous concerns about chlorine. Although chlorine disinfects drinking water, it also reacts with traces of other material of particles, such as dissolved solids, in the water and forms trace amounts of substances known as disinfection byproducts (DBPs). The most common of these are known as trihalomethanes (THMs). The United States Environmental Protection Agency (EPA) has classified THMs as a probable carcinogen.

Chlorine is said by some to be the original persistent organic pollutant (POP). POPs persist in the environment for decades and research by Columbia University suggests they may remain for centuries.

Many now-banned substances (e.g., Agent Orange, DDT, PCBs) and many others like them all have one legal cousin– chlorine. Dr. Joe Thornton, a biologist at Oregon University, states in his book Pandora’s Poison that all of the organochlorines contaminate the environment, wildlife, our food and our bodies. They have just one antidote: “ban them all”. An organochlorine is a class of chemicals formed when chlorine gas produced by the chemical industry comes into contact with organic matter in industrial processes and in agricultural uses.

There are 11,000 organochlorines that are known to exist. They are both persistent and stable in the environment, and they accumulate in the fatty tissues of animals and humans. They have been in existent since 1940 and now blanket the entire planet. Everyone on earth now eats, drinks, and breathes a constantly changing and poorly characterized soup of organochlorines, said Dr. Joe Thornton.

Organochlorines have been linked to immune system suppression, falling sperm counts and infertility, as well as learning disability in children.

Notable Quotes and Facts

  • A study by the U.S. Council of Environmental Quality showed that the cancer risk among people drinking chlorinated water is 93% higher than among those whose water does not contain chlorine.
  • Dr. Lance Wallace of the Environmental Protection Agency states that “Taking long, hot showers is a health risk exposing us to a greater extent to the toxic chemicals contained in water.”
  • Dr. Niels Skakkebaek of the University of Copenhagen conducted a study that demonstrates how the average human sperm counts have dropped in Denmark by almost 50% due to the presence of man-made chlorine found in human tissues and breast milk.
  • Dalhousie University in Nova Scotia, found that high levels of trihalomethanes, a by-product of chlorine in drinking water, significantly increased the risk of stillbirth.
  • Dr. J. M. Price states that the cause of arteriosclerosis and resulting heart attacks and strokes is none other than ubiquitous chlorine in our drinking water.
  • A professor of Water Chemistry at the University of Pittsburgh claims that exposure to vaporized chemicals in the water supplies through showering, bathing, and inhalation is 100 times greater than through drinking water.
  • The National Academy of Sciences estimate that over 1000 people die in the United States each year from cancer caused by ingesting the contaminates in water. Tens of thousands are made acutely ill.
  • Dr. Thornton warns, that the levels of dioxin in the environment can only increase, as long as organochlorines are produced. “Once we’re got them, we’re got them, and there’s no safe way of disposing of them…. Once they’re in you, there’s no way to get them out.”

Dr. Riddle suggests that since chlorine is required by health regulations to be present in all public drinking water supplies, it is up to the individual to remove the chlorine by “Point of entry systems at the home and Point of use systems” elsewhere when possible. It is not expensive to filter and with understanding of the many cautions mention in this article, all research states that all chlorine must be removed prior to consumption.

Many Valuable Uses (Worth Noting): Surely many of us would not be here if chlorine had not been used to eradicate the plagues and diseases that were prevalent prior to 1904. Your parents or grandparents might have been among those who fell victim to those water-borne diseases. It was chlorine that increased life expectancy from 45 years to 77 years.

Since 1846, when chlorine was first used as a germicide, it has become much more than most people realize. Due to its ability to combine and react with other elements and compounds, chlorine is now a key building block of modern life. Almost every product made today benefits from chlorine chemistry. Chlorine makes water safe to drink, produces life-saving drugs and medical equipment, shields police and fire fighters, protects crops, comes to the rescue in disasters, and cleans and disinfects everything in or around the home. Hotels, nursing homes, hospitals, restaurants, schools, businesses and manufacturers all depend on chlorine.

It is also completely true that what we don’t know about chlorine may harm us in numerous ways (this is a summary of a 2 part series published by Intec). For complete article, contact Intec.

Learn more about Chlorine Free Pools

More on purifying your drinking/bathing water

Chlorine and Health Risk Links

Dermal Absorption

General Health Risks


Few things tie humans so directly to the natural environment as drinking-water. The contamination of water is a direct reflection of the degree of contamination of the environment. After flushing airborne pollutants from the skies, rainwater literally washes over the entire human landscape before running into the aquifers, streams, rivers, and lakes that supply our drinking-water. Any and all of the chemicals generated by human activity can and will find their way into water supplies. Evaluating possible links between drinking-water and cancer means identifying those chemicals that appear in enough water supplies at sufficient concentrations to pose a substantial attributable cancer risk.

Contaminants may enter water supplies at many points before reaching the tap. The types and quantities of carcinogens present in drinking-water at the point of consumption may result from contamination of the source water, arise as a consequence of treatment processes, or enter as the water is conveyed to the user. Many different carcinogens may contaminate source waters, but they usually exist in drinking-water at low concentrations. On the other hand, chemicals that enter drinking-water during the course of water treatment are limited in number, but these chemicals appear in drinking-water supplies with greater frequency than most source water contaminants. Finally, the compounds contained in the pipes, joints, and fixtures of the water distribution system may contaminant treated water on its way to the consumer. Similarities in the construction of drinking-water distribution systems mean that any carcinogen entering through this pathway may be widespread and can pose substantial attributable risks of cancer. The following discussion reviews the attributable risks for contaminants entering at each of these points. Data gaps are identified and emerging areas of concern are discussed.

Source Water Contaminants

Except for naturally occurring minerals such as calcium carbonate, contaminants that enter the water supply through the source water generally occur at low concentration levels. Source water contaminants of concern either are sufficiently potent carcinogens to pose risks at extremely low concentrations or cause local contamination at high concentrations. The source-water contaminants that have been the focus of concern among those individuals investigating environmental cancer risks include arsenic, asbestos, radon, agricultural chemicals, and hazardous waste.

Some of the strongest evidence for a cancer risk associated with source-water contamination involves arsenic. Epidemiologic studies from Taiwan have suggested that arsenic in drinking-water poses substantial risks of liver, lung, bladder, and kidney cancer as listed in Table 1 (1,2). Although toxicologic studies do not provide unequivocal evidence of carcinogenicity (3), occupational studies, as well as other epidemiologic studies, support the findings of the Taiwanese studies(4). Estimates of attributable risk based on the data in Table 1 suggest that an average level of arsenic 2.5 µg/l in drinking-water in the United States of causes approximately 3000 cases of cancer per year (4).


Although asbestos is a proven carcinogen, the attributable risks associated with asbestos in drinking-water do not appear to be substantial. An early study in California (5) suggested that there may be an elevation in colorectal cancer risk associated with asbestos in drinking-water. It appears that these findings are limited to situations in which naturally occurring levels are high. A subsequent, more detailed study of asbestos in source water, together with studies of asbestos leached from water distribution systems, suggests that, when asbestos is present at levels commonly found in drinking-water, it does not pose a major cancer risk (6,7).

Radon is also a known carcinogen; however, the evidence linking consumption of radon-contaminated water to human cancer is weak (8). The relationship between ionizing radiation and cancer is well understood. This information, coupled with measured levels of radon in drinking-water, suggests that fewer than 100 cases of cancer occur each year in the United States as a consequence of consuming radon in drinking-water (9).

Farm runoff containing agricultural chemicals and manure may lead to local or regional contamination of source waters with insecticides, fungicide, rodenticides, herbicides, and fertilizers, which contain phosphorous and nitrogen. Although some pesticides are carcinogens, drinking-water contamination resulting from their agricultural application has not been directly associated with cancer in epidemiologic studies. Emerging evidence, however, indicates that fertilizers may pose cancer risks.

Studies in China among populations exposed to high levels of nitrates in drinking-water have suggested links between nitrate contamination and stomach and liver cancer (10). In these studies, the histology of the gastric lesions has been linked to the level of nitrates in the water (11) and cancer rates increased with the in vitro mutagenicity of the drinking-water (12). Nitrates may act as carcinogens through the formation of N-nitroso compounds (13). When human volunteers were given proline, which is a secondary amine, those participants in areas with higher levels of nitrate in their drinking-water had higher levels of N-nitrosoproline in their urine than volunteers residing in places with low nitrate levels in their drinking-water (14). Although an epidemiological study in France failed to demonstrate an association between nitrates in drinking-water and cancer (15), current evidence is sufficient to warrant further study of this potential carcinogen.

Few examples of significant links between hazardous waste in drinking-water and cancer have been reported. Elevated cancer risks are difficult to detect because of the relatively low incidence of site-specific neoplasms and the typically small size of exposed populations (16). An ecologic study in New Jersey found weak evidence for a positive association between volatile organic compounds in drinking-water and leukemia (17). In a national ecologic study, Griffith et al. (18) found evidence of elevated cancer rates in the vicinity of hazardous waste sites. Limitations on ecologic data urge caution in the interpretation of such findings. Contamination of wells associated with hazardous waste disposal in Woburn, Massachusetts, was ultimately linked to elevations in their incidence of leukemia (19). Although this investigation was arguably the most thorough study of this kind, questions were raised about the magnitude of the risk (20). There are numerous factors that make it difficult, if not impossible, to estimate the attributable risks associated with hazardous wastes on a national level, including the wide variety of chemicals present in hazardous waste sites, the difficulties in assessing exposure, the obstacles to establishing links between exposure and cancer even when links are present, the small size of exposed populations, and the uncertainties concerning future risks.

Cancer Risks Associated with Water Treatment

Until this century, concerns about the cleanliness of drinking-water focused almost exclusively on the presence or absence of pathogens. Ironically, the chlorine used to reduce the risk of infectious disease may account for a substantial portion of the cancer risk associated with drinking-water.

Chlorination of drinking-water played a central role in the reduction in the mortality rates associated with waterborne pathogens. Water chlorination was first introduced at the Jersey City Water Works in Boonton, New Jersey. The relative ease of use of water chlorination, together with its potent bactericidal action, lead to the rapid dissemination of this treatment technology throughout the United States. Overshadowed by the clear benefits to public health, the potential health risks associated with water chlorination received little attention. This view is evident in an article heralding the opening of the Boonton waterworks, which appeared on the back page of the New York Times (21). The brief article claimed that, with this process, “any municipal water supply can be made as pure as mountain spring water. Chlorination destroys all animal and microbial life, leaving no trace of itself afterwards” (21).

This statement represented the prevailing wisdom until about 20 years ago when halogenated organic compounds, particularly chloroform, were identified in chlorinated drinking-water (22). A subsequent survey of water supplies showed that these compounds were common in water supplies throughout the United States and that concentrations were far higher in treated surface water than in treated groundwater (23). With these revelations came a shift in the basis of our definition of cleanliness in drinking-water. New concerns about cancer risks associated with chemical contamination from chlorination by-products have given rise to 25 epidemiologic studies.

Table 2 summarizes the results of a metaanalysis of the cohort and case-control studies that have been conducted to evaluate the association between consumption of chlorinated drinking-water and cancer at various sites (24). For each cancer site, the pooled results from available studies show elevations in risk, and the risk estimates achieved statistical significance for bladder and rectal cancer. Further analyses in this study suggested that risks increased with increasing exposure and that improvements in exposure assessment yielded higher estimates of risk. Confounding could conceivably explain the observed pattern of association, but stratification into studies that adjusted or did not adjust for confounders does not support such an assertion. Studies that adjusted for population density, smoking, or occupation, did not demonstrate a difference in relative risk estimates. Although it is still possible that the pattern of associations could represent some systematic bias in the available studies, no specific bias has emerged to explain the observed results.


In summary, the available studies generally support the notion that by-products of chlorination are associated with increased cancer risks. The precise characterization of these risks is somewhat less clear. The broad category of chlorination by-products includes many different compounds, and the carcinogens among these compounds have not been clearly identified. Trihalomethanes are the most prevalent compounds and, given the evidence suggesting that they are animal carcinogens, have been the focus of research and regulation. The chlorination by-products that have been specifically identified, however, account for only about half of the bound chlorine in finished drinking-water. Other compounds present in far smaller quantities may pose substantial cancer risks by virtue of high potency (25).

The goal of precise characterization of the cancer risk posed by each of the chlorination by-products will probably prove to be unrealistic. A quantitative dose-response relationship has not been well described for any individual compound, much less the entire complex mixture. The relative contributions of different exposure pathways vary among the by-products and have not been well characterized. Nonetheless, given the large number of people who consume chlorinated surface water, the number of cases of cancer potentially attributable to this exposure is substantial. The numbers derived from the metaanalysis suggest that 5000 (95% CI=2000-7000) cases of bladder cancer per year and 8000 cases of rectal cancer per year (95% CI=200-14,000) may be associated with consumption of chlorinated drinking-water. Although these figures do not provide a precise estimate of risk, the true risk is probably within an order of magnitude of these values.

Since the publication of the meta-analysis, a number of other studies have been completed. McGeehin et al. (26) found an elevated risk for bladder cancer comparable in magnitude to the summary estimate of the metaanalysis. Kuovaslo et al. (27) found a similar estimate of risk for bladder cancer but did not find an elevated risk for rectal cancer. Kantor (28), on the other hand, found a risk for rectal cancer similar to that in the metaanalysis, but an increase in bladder cancer risk associated with chlorination by-products was only observed among smokers. Including these findings within the metaanalysis does not change its results. Nonetheless, these apparent inconsistencies may reflect important differences in the carcinogenicity of the exposures experienced among the various study populations. The complex mixture of compounds that comprise chlorination by-products, the multiple pathways of exposure to those compounds, and the potential for synergy with diet and other exposures may well explain the apparent inconsistencies that exist among the studies included in the metaanalysis.

To stop chlorination of drinking-water to eliminate the elevated cancer risks from chlorination by-products would be foolhardy. Nonetheless, the data provide strong evidence to support expanded efforts in research and development of alternatives to chlorination for the disinfection of drinking-water. Chlorination is particularly effective in preventing recontamination during distribution. Alternatives must provide a similar level of protection. The capacity of chemical disinfectants to kill pathogens generally reflects their strong tendency to react with organic chemicals. The production of by-products may, therefore, be inherent to the chemical disinfection of drinking-water. For example, ozone produces aldehydes including formaldehyde and bromate if the source waters contain bromine. These compounds pose a cancer risk that is not yet fully quantified (29). Before the widespread introduction of any new method of water treatment, the carcinogenicity of by-products should be carefully evaluated.

Of the other compounds routinely added during the course of drinking-water treatment, fiuoride has received the greatest scrutiny as a potential carcinogen. The International Agency for Research on Cancer (IARC) working group on cancer risks from fluoridated drinking-water has concluded that available ecologic studies have been consistent in finding no risk but stopped short of suggesting that flouride was not carcinogenic because the studies were all ecologic in design (30). One animal study (31) and one case-control study (32) suggested that fluoridated water could be linked with osteosarcoma, but these findings will require further confirmation to be considered suggestive of causality. It appears that if flouride poses any cancer risk, the attributable risk is relatively small.

Cancer Risks Associated with Drinking-water Distribution

The chemical components of pipes, joints, and fixtures can contaminate drinking-water after treatment. A broad range of materials are used in these systems. Pipes can be made from metals, primarily iron, copper and lead; plastics, such as polyvinyl chloride and polyethylene; and concrete or asbestos/concrete aggregates. These pipes may be plated or lined with a variety of compounds including zinc, coal tar, asphalt, or vinyl. In addition, bacteria and organic matter frequently coat the inside of pipes within the distribution systems (33). All of these can be sources of new contamination, or they can combine with chemicals already in the water to alter the health risks posed by drinking-water. In 1979, a study of several medium-size water systems demonstrated increases in mutagenicity of drinking-water after passage through the distribution system (34). This study did not isolate specific contaminants that might be responsible. Perhaps the most extensively studied contaminant associated with drinking-water distribution is asbestos, which can leach from asbestos-concrete pipes. The available research suggests that asbestos from this source does not pose significant human cancer risks (3537). A study by Ashengrau et al. (38) showed an increase in leukemia in association with trichlorethylene, which had leached from a plastic liner used in concrete pipes. Other than the negative results of the asbestos studies, the available research does not allow for strong conclusions concerning the magnitude of cancer risks relating to contamination from the distribution system. Further research is needed to identify and quantify risks posed by contamination that occurs during drinking-water distribution.

Emerging Concerns and Potential Cancer Risks

Water is among the most basic requirements for human survival, therefore, emerging health threats related to drinking-water contamination demand careful consideration. Although the identification of potential threats to human health requires a certain degree of speculation, protection of public health requires a willingness to occasionally err in the name of caution. Cancer risks may emerge from the micropollutants and microbial contaminants that can enter our drinking-water supply. Less direct effects may also pose risks.

One focus of current concerns about the potential for micropollutants to cause cancer involves those compounds that mimic naturally occurring, biologically active compounds. Biologically active micropollutants or endocrine disrupters appear to have the ability to disturb normal intercellular communications. For example, evidence from wildlife biologists, toxicologists, endocrinologists, and epidemiologists demonstrate the potential for estrogenic effects of environmental contaminants among humans (39,40). Metabolites of DDT are estrogenic in vivo and have been associated with the development of breast cancer in epidemiologic studies (41,42). Nonyl-phenol, a common chemical surfactant, increases proliferation in breast tumor cell cultures (43). The potential risks from drinking-water contaminants acting through these mechanisms have not been evaluated.

Because of the complex mixture of contaminants, examining cancer risks for each individual compound may not give a complete picture of cancer risks associated with drinking-water. An alternative approach is to look at the geographic distribution of neoplasms that might be associated with drinking-water. These include cancer of the gastrointestinal tract and bladder cancer (i.e., neoplasms of the mucosal epithelium). Figure 1 provides maps showing clustering of the incidence of site-specific neoplasms among the elderly. By ranking the incidence of the neoplasms of the mucosal epithelium and combining those ranks, we can see where this group of neoplasms might be elevated. A map of the clustering of elevated cancer rates is shown in Figure 2. This map indicates a significant elevation of these cancers in the northeastern United States. To draw conclusions about the link between the geographic distribution and drinking-water would, of course, be premature, but any effort to explain this pattern should consider drinking-water contamination to be a possible contributing factor.


Figure 1. Rank sum map of incidence rates among persons 65 and older for cancers of the esophagus, stomach, colon, rectum, and bladder from 1988 to 1989 (Based on Appendix I).


Figure 2. Areas of significant clustering of elevated rates of mucosal neoplasms. Significance of Moran’s I: p<0.0001.

Microbial contaminants also have carcinogenic potential. For example, Schistosoma haematobium is waterborne, although it is not transmitted by drinking-water, and has been linked to cancer of the urinary bladder (44). Tumor promotion by algal toxins has already been suggested in literature (45). Bacteria, parasites, and viruses appear sporadically in most water supplies. The possibility that currently unidentified pathogens in drinking-water can cause cancer should not be overlooked.

Water pollution may pose cancer risks other than the direct, toxic effects of exposure to contaminated water. Causal links for the effects described below have not been clearly established, but they are plausible and should be considered in evaluating cancer risks from drinking-water.

Contamination of fishing grounds may pose both direct and indirect cancer risks. Persistent, potentially carcinogenic compounds, such as polychlorinated biphenyls, accumulate in the fatty tissues of fish (46). Fish consumption is a major exposure pathway for these compounds. In addition, contamination or destruction of spawning grounds may combine with over-fishing to deplete natural fisheries. A dietary shift from fish to red meat, either because of diminished fish stocks or fear of contaminants, could also increase diet-associated cancer risks.

Under conditions of average temperature, humidity, and activity, the human body loses and, therefore, must replace about 2.3 liters of water each day. Two-thirds of this consumption is in the form of water or some other beverage. Concerns about the health risks or taste of drinking-water may induce those who consume tap water to shift to bottled water, or other beverages. These beverages may include sweetened soft drinks and alcoholic beverages, which can pose health risks greater than those associated with drinking-water. In addition, the production and disposal of containers for alternative beverages, including bottled water may lead to the release of carcinogens.

Summary and Prevention Strategies

The cancer risks associated with the major contaminants of drinking-water are listed in Table 3. The weight of the evidence suggests that chlorination by-products pose substantial cancer risks that should be reduced. A growing body of evidence supports the possibility that arsenic in drinking-water may also carry unacceptable cancer risks. The cancer risks from radon and asbestos in drinking-water are less substantial but may require remediation where local conditions dictate. The available evidence does not support assertions of cancer risks associated with fluoridation of drinking-water.


For most other compounds present in drinking-water, the attributable cancer risks are not clear. Hazardous waste and pesticides may contaminate waters locally and regionally, but the attributable cancer risk is difficult to quantify. Nitrates are more widespread contaminants and more closely linked to human cancer, but evidence is incomplete. Contamination during drinking-water distribution may pose cancer risks, but the epidemiologic evidence is extremely limited. Less conventional cancer risk factors, such as biologically active micro pollutants and pathogens, only present the possibility of risk at present but may emerge as important carcinogens in the future.

Cancer-prevention strategies must focus on source-water purity. In particular, strong source-water protection efforts provide a barrier to emerging cancer risks that have not been identified or fully characterized. Furthermore, failure to protect source water purity will necessitate more extensive water treatment and, in most cases, heavier chlorination. Drinking-water treatment technologies should be evaluated with extreme care and should be reevaluated on a regular basis. The concept of continuous quality improvement should be fully integrated into drinking-water treatment and should include ongoing efforts to develop, evaluate, and implement new treatment technologies. More cost-effective methods for monitoring drinking-water quality need to be aggressively developed. Finally, drinking-water research should be a priority. The consequences of a lack of vigilance with respect to emerging threats in drinking-water were felt with devastating impact in Milwaukee, Wisconsin, in 1993, when 400,000 people fell ill during a waterborne outbreak of cryptosporidiosis (47). We should view this as a warning and an opportunity for timely intervention to minimize health risks from drinking-water.

Appendix I

The map of cancer incidence rates for mucosal cancer was based on the application of the method described below.

Assessing Cancer Incidence Rates

The incidence of cancer of the esophagus, stomach, colon, and urinary bladder for persons over 64 years of age for the period 1988 through 1989 was estimated using Medicare hospital admissions data. The method used to estimate cancer incidence with this database is reported elsewhere (1-3). Briefly stated, all patients with a hospital admission for cancer were identified. Patients with no admissions for the site specific cancer diagnosis in the previous 4 years were considered to represent incident cases. From these, age and sex adjusted, race-specific cancer rates were determined.

Localizing Disease Clusters

A disease cluster can be defined as a group of geographic areas that are close to one another with disease rates that are similarly increased or decreased relative to surrounding areas. This can be expressed quantitatively for each analytic area i, as the weighted covariance of its disease rate (xi) with the rates for the rest of the analytic areas in the study region (xj) as given by

116x46 [1]

where the weights (wij) are the inverse of the distance between population centroids of the analytic areas (4).

If the sizes of the study areas are not homogeneous across the study regions, the weights corresponding to two adjacent areas will vary according to the size of those areas. After modification to accommodate variations in region size, the regional spatial autocorrelation coefficient (RSAC) for analytic area i, Ri, becomes,

216x68 [2]

The mean and standard deviation of the distribution of RSAC can be reasonably approximated by a normal distribution with an expectation of zero and a standard deviation of O/(n-2)1/2 where O is the standard deviation of xi and n is the number of analytic areas.

The RSAC was calculated for each analytic area, and the theoretical mean and standard deviation were used to test for significance. Analytic areas that have significantly high RSACs were further classified into two groups based on whether their disease rates were greater or less than the median rate. Analytic areas with significant RSACs and disease rates greater than the median were defined as analytic areas with clustering of elevated disease rates or high clusters. These analytic areas were shaded black in the map. Analytic areas with significant RSACs and disease rates less than the median were defined as analytic areas with clustering of low disease rates or low clusters. When the value of the RSAC was not significant, analytic areas were not shaded and represented random spatial structures. Maps depicting the results of these analyses (RSAC maps) were created to evaluate the use of this method as a visual aid to localize areas that contain disease clusters. These methods are described in detail elsewhere (1,4). The resulting maps are shown in Figure Al.


Figure A1. Regional spatial autocorrelation coefficient (RSAC) maps showing localized areas containing statistically significant disease clusters. (A) Malignant neoplasm of the esophagus. (B) Malignant neoplasm of the bladder. (C) Malignant neoplasm of the colon. (D) Malignant neoplasm of the stomach. Significance of Moran’s I: p<0.0001.


from Intec-America

What are biofilms? Biofilms are a complex matrix of bacteria, fungi, and algae bound together in a sticky gel of polysaccharide and other organic contaminants attached to a surface. The bacteria produce a slime layer in which they live that anchors them firmly to a surface and which provides a protective environment to grow and reproduce. Biofilms generally form on any wet surface and are consequently found in many types of environments, especially poultry drinking water systems. Biofilms harbor harmful microorganisms such as Campylobacter, Listeria, Salmonella, E. Coli, Pseudomonas, and Staphylococcus. The existence of biofilm reduces the effectiveness of common disinfectants.

As previously stated, poultry watering systems harbor biofilms. Water sources, such as well or surface water that contain high mineral content, iron bacteria, or coliform, may produce biofilms. The use of vitamins or other sugar based products (Gatorade, Kool-Aid, etc.) is a food source for the microorganisms and will promote the formation of biofilms as well. Problems associated with biofilms in the poultry drinking water include a decrease in poultry survival time, lowered egg production, deterioration of equipment, and clogging of nipple drinkers. Utilizing public water systems or a applying a disinfectant throughout the grow-out (Chlorine gas, chlorine dioxide/anthium dioxide, iodine, or ozone) will not make a farm immune to these biofilm.

Traditional disinfectants do not effectively penetrate the biofilm matrix. The disinfectant must have access to the bacteria in order to be effective. Most disinfectants are active against planktonic (unattached) microorganisms but are not effective against microorganisms in biofilm. In order to penetrate and remove biofilms, it is necessary to hydrolyze the biofilm matrix. Hydrolysis breaks up the biological material and exposes the microorganisms within it to the killing action of disinfecting agents. Below are some products commonly utilized in the industry that are not effective against biofilm:

  • Quats are surface antimicrobials. They have no chemical reactivity with biofilm polysaccharide and are bound up by negative charge on the biofilm surface. Quats leave much of the biofilm matrix intact and do not remove or destroy endotoxins.
  • Chlorine Dioxide is a strong oxidizing agent. Chlorine Dioxide reacts with the surface of the biofilm but provides no hydrolytic breakdown of the biofilm matrix or mechanical removal.
  • Peracetic Acid is active on surface regions of biofilm, but is rapidly neutralized by catalase. There is no hydrolysis or mechanical breakdown of biofilm matrix polysaccharides.
  • Citric acid, muriatic acid, sodium hydrogen sulfate, and other acidifiers used to lower pH are neither approved biocides (ability to kill microorganisms) nor biodispersants (ability to penetrate and remove biofilms). These products are effective at removing scale as discussed later.

It is recommended that poultry water lines be cleaned and disinfected with a product that has EPA-registered claims to penetrate and remove biofilm, and to kill biofilm bacteria. Such a product has passed EPA-required tests that establish the efficacy of the product in removing and penetrating biofilm from surfaces and water lines. The above-mentioned quaternary ammonium products, chlorine dioxide, and peracetic acid do not have EPA-registered claims to penetrate and remove biofilms. Some products may carry an EPA registration for a being biocide and are labeled as cleaners. Only evaluation of the product’s label will determine which product is EPA approve for biofilm removal or if it simply kills microorganisms.

What is scale and how is it caused? Hard water is usually associated with well water in regions where the rocks contain a large proportion of minerals such as calcium and magnesium, principally as bicarbonates, and sometimes iron and manganese. Over time, water containing these minerals will attach to plumbing and form scale. Harder scale is comprised of iron and manganese and is more difficult to remove. Softer scale is comprised mostly of calcium and magnesium and is easier to remove. The pH of the water will also play an important role in the formation of scale, where water with a higher pH (over 7.0) will form harder scale at a faster rate. Water with a lower pH will tend to have a mineral “sludge” present in the lines.

There are several concerns associated with mineral scale. Economic impacts to the grower include clogged plumbing and regulators, pressure loss, and nipple drinkers sticking or leaking. Over time, this is a substantial cost when one considers the time and money of replacement. Pretreated water (i.e. filtered or softened water), is a cost effective means of reducing/preventing future problems.

Scale has a rough surface that contains pitting, cracks, and crevices which can harbor microorganisms. Disinfectants such as chlorine and iodine simply pass over these cracks and crevices and the microorganisms will continue to flourish. Therefore, additional treatment measures must be used.

To remove the scale, the pH of the water must be reduced by adding an acid to dissolve the mineral scale. However, the biofilm has to be removed first. An acid can not fully penetrate and will not hydrolyze the biofilm and thus can not dissolve the scale. Consequently, a product with EPA-registered claims to penetrate and remove biofilm must be used before scale can be dissolved. Follow the instruction of the acid product manufacturer for proper use and safety guidelines. The influent pH of the water should also be considered. Water with a natural pH of 8.5 requires the use of more acid than water with a natural pH of 7.2.

There is a common misconception that chlorinated water does not require any maintenance and lines do not have to be flushed. This is absolutely false. Public water, treated well or surface water may reduce the severity of contamination in the lines. However, the lines still remain susceptible to biofilm formation. Regardless of the water quality or water source, it is highly encouraged to clean the water lines between flocks. The grower will realize significantly higher productivity and profits over time with a proactive versus a reactive program.

Any farm that has included water in its Biosecurity program and follows the quality assurance measures set in place by the company’s veterinarian will have a distinct advantage over those that do not. Poultry production is more competitive than ever before and clean water will surely make a difference in the profitability for the grower.