# ![](media/image1.wmf)Disinfectant Use in Water Treatment

To comply with the SDWA regulations, the majority of PWSs use some form
of water treatment. The 1995 Community Water Systems Survey (USEPA,
1997a) reports that in the United States, 99 percent of surface water
systems provide some treatment to their water, with 99 percent of these
treatment systems using disinfection/oxidation as part of the treatment
process. Although 45 percent of ground water systems provide no
treatment, 92 percent of those ground water plants that do provide some
form of treatment include disinfection/oxidation as part of the
treatment process. The most commonly used disinfectants/oxidants (in no
particular order) are chlorine, chlorine dioxide, chloramines, ozone,
and potassium permanganate.

Disinfectants are also used to achieve other specific objectives in
drinking water treatment. These other objectives include nuisance
control (e.g., for zebra mussels and Asiatic clams), oxidation of
specific compounds (i.e., taste and odor causing compounds, iron, and
manganese), and use as a coagulant and filtration aid.

The purpose of this chapter is to:

-   Provide a brief overview of the need for disinfection in water
    treatment.

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-   Provide basic information that is common to all disinfectants;

-   Discuss other uses for disinfectant chemicals (i.e., as oxidants);

-   Describe trends in DBP formation and the health effects of DBPs
    found in water treatment;

-   Discuss microorganisms of concern in water systems, their associated
    health impact, and the inactivation mechanisms and efficiencies of
    various disinfectants; and

-   Summarize current disinfection practices in the United States,
    including the use of chlorine as a disinfectant and an oxidant.

## Need for Disinfection in Water Treatment

Although the epidemiological relation between water and disease had been
suggested as early as the 1850s, it was not until the establishment of
the germ theory of disease by Pasteur in the mid-1880s that water as a
carrier of disease-producing organisms was understood. In the 1880s,
while London experienced the "Broad Street Well" cholera epidemic, Dr.
John Snow conducted his now famous epidemiological study. Dr. Snow
concluded that the well had become contaminated by a visitor, with the
disease, who had arrived in the vicinity. Cholera was one of the first
diseases to be recognized as capable of being waterborne. Also, this
incident was probably the first reported disease epidemic attributed to
direct recycling of non-disinfected water. Now, over 100 years later,
the list of potential waterborne diseases due to pathogens is
considerably larger, and includes bacterial, viral, and parasitic
microorganisms, as shown in Table 2-1, Table 2-2 and Table 2-3,
respectively.

A major cause for the number of disease outbreaks in potable water is
contamination of the distribution system from cross connections and back
siphonage with non-potable water. However, outbreaks resulting from
distribution system contamination are usually quickly contained and
result in relatively few illnesses compared to contamination of the
source water or a breakdown in the treatment system, which typically
produce many cases of illnesses per incident. When considering the
number of cases, the major causes of disease outbreaks are source water
contamination and treatment deficiencies (White, 1992). For example, in
1993 a Cryptosporidiosis outbreak affected over 400,000 people in
Milwaukee, Wisconsin. The outbreak was associated with deterioration in
the raw water quality and a simultaneous decrease in the effectiveness
of the coagulation-filtration process (Kramer et al.*,* 1996; MacKenzie
et al.*,* 1994). Historically, about 46 percent of the outbreaks in the
public water systems are found to be related to deficiencies in source
water and treatment systems with 92 percent of the causes of illness due
to these two particular problems.

All natural waters support biological communities. Because some
microorganisms can be responsible for public health problems, biological
characteristics of the source water are one of the most important
parameters in water treatment. In addition to public health problems,
microbiology can also affect the physical and chemical water quality and
treatment plant operation.

### Pathogens of Primary Concern

Table 2-4 shows the attributes of three groups of pathogens of concern
in water treatment, namely bacteria, viruses, and protozoa.

#### Bacteria

Bacteria are single-celled organisms typically ranging in size from 0.1
to 10 μm. Shape, components, size, and the manner in which they grow can
characterize the physical structure of the bacterial cell. Most bacteria
can be grouped by shape into four general categories: spheroid, rod,
curved rod or spiral, and filamentous. Cocci*,* or spherical bacteria,
are approximately 1 to 3 μm in diameter. Bacilli (rod-shaped bacteria)
are variable in size and range from 0.3 to 1.5 μm in width (or diameter)
and from 1.0 to 10.0 μm in length. Vibrios, or curved rod-shaped
bacteria, typically vary in size from 0.6 to 1.0 μm in width (or
diameter) and from 2 to 6 μm in length. Spirilla (spiral bacteria) can
be found in lengths up to 50 μm whereas filamentous bacteria can occur
in length in excess of 100 μm.

[]{#__RefHeading___Toc450037295 .anchor}Table 2-1. Waterborne Diseases
from Bacteria

+-----------+-------+--------------------------------+----------------+
| **        | *     | **Symptoms**                   | **Reservoir**  |
| Causative | *Dise |                                |                |
| Agent**   | ase** |                                |                |
+-----------+-------+--------------------------------+----------------+
| *S        | Ty    | Headache, nausea, loss of      | Feces and      |
| almonella | phoid | appetite, constipation or      | urine of       |
| typhosa*  | Fever | diarrhea, insomnia, sore       | typhoid        |
|           |       | throat, bronchitis, abdominal  | carrier or     |
|           |       | pain, nose bleeding, shivering | patient.       |
|           |       | and increasing fever. Rose     |                |
|           |       | spots on trunk. Incubation     |                |
|           |       | period: 7-14 days.             |                |
+-----------+-------+--------------------------------+----------------+
| *S.       | P     | General infection              | Feces and      |
| p         | araty | characterized by continued     | urine of       |
| aratyphi* | phoid | fever, diarrhea disturbances,  | carrier or     |
|           | fever | sometimes rose spots on trunk. | patient.       |
| *S.       |       | Incubation period: 1-10 days.  |                |
| schott    |       |                                |                |
| inulleri\ |       |                                |                |
| S.        |       |                                |                |
| hir       |       |                                |                |
| schfeldi* |       |                                |                |
| C.        |       |                                |                |
+-----------+-------+--------------------------------+----------------+
| *Shigella | Baci  | Acute onset with diarrhea,     | Bowel          |
| flexneri\ | llary | fever, tenesmus and stool      | discharges of  |
| Sh.       | dyse  | frequently containing mucus    | carriers and   |
| dys       | ntery | and blood. Incubation period:  | infected       |
| enteriae\ |       | 1-7 days.                      | persons.       |
| Sh.       |       |                                |                |
| sonnei\   |       |                                |                |
| Sh.       |       |                                |                |
| paradys   |       |                                |                |
| interiae* |       |                                |                |
+-----------+-------+--------------------------------+----------------+
| *Vibrio   | Ch    | Diarrhea, vomiting, rice water | Bowel          |
| comma\    | olera | stools, thirst, pain, coma.    | discharges,    |
| V.        |       | Incubation period: a few hours | vomitus,       |
| cholerae* |       | to 5 days.                     | carriers.      |
+-----------+-------+--------------------------------+----------------+
| *Pa       | Tula  | Sudden onset with pains and    | Rodent,        |
| steurella | remia | fever; prostration. Incubation | rabbit,        |
| tu        |       | period: 1-10 days.             | horsefly,      |
| larensis* |       |                                | woodtick, dog, |
|           |       |                                | fox, hog.      |
+-----------+-------+--------------------------------+----------------+
| Brucella  | B     | Irregular fever, sweating,     | Tissues,       |
| m         | rucel | chills, pain in muscles.       | blood, mold,   |
| elitensis | losis |                                | urine,         |
|           | (und  |                                | infected       |
|           | ulant |                                | animal.        |
|           | f     |                                |                |
|           | ever) |                                |                |
+-----------+-------+--------------------------------+----------------+
| Ps        | M     | Acute diarrhea, vomiting, high | Rats, guinea   |
| eudomonas | elioi | fever, delirium, mania.        | pigs, cats,    |
| pse       | dosis |                                | rabbits, dogs, |
| udomallei |       |                                | horses.        |
+-----------+-------+--------------------------------+----------------+
| *L        | Lep   | Fevers, rigors, headaches,     | Urine and      |
| eptospira | tospi | nausea, muscular pains,        | feces of rats, |
| i         | rosis | vomiting, thirst, prostration  | swine, dogs,   |
| cterohaem | (W    | and jaundice may occur.        | cats, mice,    |
| orrhagiae | ell's |                                | foxes, sheep.  |
| (spiroch  | dis   |                                |                |
| aetales)* | ease) |                                |                |
+-----------+-------+--------------------------------+----------------+
| Enterop   | Gastr | Water diarrhea, nausea,        | Feces of       |
| athogenic | oente | prostration and dehydration.   | carrier.       |
| *E. coli* | ritis |                                |                |
+-----------+-------+--------------------------------+----------------+
|           |       |                                |                |
+-----------+-------+--------------------------------+----------------+

Sources: Salvato, 1972; Geldreich, 1972.

[]{#__RefHeading___Toc450037296 .anchor}Table 2-2. Waterborne Diseases
from Human Enteric Viruses

+-----+-----+------+-------------+-------------------+----------------+
| **G | **S | *    | **Disease   | **Pathological    | **Organs Where |
| rou | ubg | *No. | Entities    | Changes in        | Virus          |
| p** | rou | of   | Associated  | Patients**        | Multiplies**   |
|     | p** | T    | with These  |                   |                |
|     |     | ypes | Viruses**   |                   |                |
|     |     | or   |             |                   |                |
|     |     | Su   |             |                   |                |
|     |     | btyp |             |                   |                |
|     |     | es** |             |                   |                |
+-----+-----+------+-------------+-------------------+----------------+
| En  | P   | 3    | Muscular    | Destruction of    | Intestinal     |
| ter | oli |      | paralysis\  | motor neurons\    | mucosa, spinal |
| ovi | ovi |      | Aseptic     | Inflammation of   | cord, brain    |
| rus | rus |      | meningitis\ | meninges from     | stem\          |
|     |     |      | Febrile     | virus\            | Meninges\      |
|     |     |      | episode     | Viremia and viral | Intestinal     |
|     |     |      |             | multiplication    | mucosa and     |
|     |     |      |             |                   | lymph          |
+-----+-----+------+-------------+-------------------+----------------+
|     | Ech | 34   | Aseptic     | Inflammation of   | Stem\          |
|     | ovi |      | meningitis\ | meninges from     | Intestinal     |
|     | rus |      | Muscular    | virus\            | mucosa, spinal |
|     |     |      | paralysis\  | Destruction of    | cord, brain\   |
|     |     |      | Guill       | motor neurons\    | Spinal cord\   |
|     |     |      | ain-Barre's | Destruction of    | Skin\          |
|     |     |      | S           | motor neurons\    | Respiratory    |
|     |     |      | yndrome^1^\ | Dilation and      | tracts and     |
|     |     |      | Exanthem\   | rupture of blood  | lungs\         |
|     |     |      | Respiratory | vessels\          | Ga             |
|     |     |      | diseases\   | Viral invasion of | strointestinal |
|     |     |      | \           | parenchymiatous   | tract          |
|     |     |      | Diarrhea\   | of respiratory    |                |
|     |     |      | Epidemic    | tracts and        | Respiratory    |
|     |     |      | myalgia\    | secondary         | tract and      |
|     |     |      | P           | inflammatory      | ga             |
|     |     |      | ericarditis | responses\        | strointestinal |
|     |     |      | and         | intestinal        | tract          |
|     |     |      | m           | infections\       |                |
|     |     |      | yocarditis\ | Not well known\   | Pericardial    |
|     |     |      | \           | Viral invasion of | and myocardial |
|     |     |      | Hepatitis   | cells with        | tissue         |
|     |     |      |             | secondary         |                |
|     |     |      |             | inflammatory      | Liver          |
|     |     |      |             | responses\        |                |
|     |     |      |             | Invasion of       |                |
|     |     |      |             | parenchyma cells  |                |
+-----+-----+------+-------------+-------------------+----------------+
|     | Cox | \>24 | He          | Viral invasion of | Mouth          |
|     | sac |      | rpangina^2^ | mucosa with       |                |
|     | kie |      |             | secondary         |                |
|     | -vi |      |             | inflammation      |                |
|     | rus |      |             |                   |                |
+-----+-----+------+-------------+-------------------+----------------+
|     | A   |      | Acute       | Sore throat,      | Lymph nodes    |
|     |     |      | lymphatic   | pharyngeal        | and pharynx\   |
|     |     |      | p           | lesions\          | Meninges\      |
|     |     |      | haryngitis\ | Inflammation of   | Intestinal     |
|     |     |      | Aseptic     | meninges from     | mucosa, spinal |
|     |     |      | meningitis\ | virus\            | cord, brain    |
|     |     |      | Muscular    | Destruction of    | stem\          |
|     |     |      | paralysis\  | motor neurons\    | Skin of        |
|     |     |      | Hand        | Viral invasion of | hands-feet,    |
|     |     |      | -foot-mouth | skin cells of     | and much of    |
|     |     |      | disease^3^\ | hands-feet-mouth\ | mouth\         |
|     |     |      | Respiratory | Viral invasion of | Respiratory    |
|     |     |      | disease\    | parenchymiatous   | tracts and     |
|     |     |      | \           | of respiratory    | lungs\         |
|     |     |      | Infantile   | tracts and        | \              |
|     |     |      | diarrhea\   | secondary         | Intestinal     |
|     |     |      | Hepatitis\  | inflammatory      | mucosa\        |
|     |     |      | P           | responses\        | Liver\         |
|     |     |      | ericarditis | Viral invasion of | Pericardial    |
|     |     |      | and         | cells of mucosa\  | and myocardial |
|     |     |      | myocarditis | Invasion of       | tissue         |
|     |     |      |             | parenchyma cells\ |                |
|     |     |      |             | Viral invasion of |                |
|     |     |      |             | cells with        |                |
|     |     |      |             | secondary         |                |
|     |     |      |             | inflammatory      |                |
|     |     |      |             | responses         |                |
+-----+-----+------+-------------+-------------------+----------------+

^1^ Ascending type of muscular paralysis

^2^ Febrile episode with sores in mouth

^3^ Rash and blister on hand-foot-mouth with fever

Table 2-2. Waterborne Diseases from Human Enteric Viruses (Continued)

  ------------- -------------- ------ ----- --- ------------ ------------------ ---------------------- ------------- ----------------- ------------------- -------------------- -------------- ------------- ----------------
  **Group**     **Subgroup**                    **No. of                                               **Disease                                           **Pathological                                    **Organs Where
                                                Types or                                               Entities                                            Changes in                                        Virus
                                                Subtypes**                                             Associated                                          Patients**                                        Multiplies**
                                                                                                       with These                                                                                            
                                                                                                       Viruses**                                                                                             

  Enterovirus                  B            6                                   Pleurodynia^4^\                                        Viral invasion of                                       Intercostal   
  (continued)                                                                   Aseptic meningitis\                                    muscle cells\                                           muscles\      
                                                                                Muscular paralysis\                                    Inflammation of                                         Meninges\     
                                                                                Meningoencephalitis\                                   meninges from                                           Intestinal    
                                                                                Pericarditis,                                          virus\                                                  mucosa,       
                                                                                endocarditis,                                          Destruction of                                          spinal cord,  
                                                                                myocarditis\                                           motor neurons\                                          brain stem\   
                                                                                Respiratory disease\                                   Viral invasion of                                       Meninges and  
                                                                                \                                                      cells\                                                  brains\       
                                                                                Hepatitis or Rash\                                     Viral invasion of                                       Pericardial   
                                                                                Spontaneous abortion\                                  cells with                                              and           
                                                                                Insulin-dependent                                      secondary                                               myocardial    
                                                                                diabetes\                                              inflammatory                                            tissue\       
                                                                                Congenital heart                                       responses\                                              \             
                                                                                anomalies                                              Viral invasion of                                       Respiratory   
                                                                                                                                       parenchymiatous of                                      tracts and    
                                                                                                                                       respiratory tracts                                      lungs\        
                                                                                                                                       and secondary                                           \             
                                                                                                                                       inflammatory                                            Liver\        
                                                                                                                                       responses\                                              Placenta\     
                                                                                                                                       Invasion of                                             Langerhan's   
                                                                                                                                       parenchyma cells\                                       cells of      
                                                                                                                                       Viral invasion of                                       pancreases\   
                                                                                                                                       vascular cells\                                         Developing    
                                                                                                                                       Viral invasion of                                       heart         
                                                                                                                                       insulin-producing                                                     
                                                                                                                                       cells\                                                                
                                                                                                                                       Viral invasion of                                                     
                                                                                                                                       muscle cells                                                          

  Reovirus                                  6                                   Not well known                                         Not well known                                                        

  Adenovirus                          31                     Respiratory                                             Viral invasion of                                          Respiratory                  
                                                             diseases\                                               parenchymiatous                                            tracts and                   
                                                             \                                                       of respiratory                                             lungs\                       
                                                             Acute                                                   tracts and                                                 \                            
                                                             conjunctivitis\                                         secondary                                                  Conjunctival                 
                                                             \                                                       inflammatory                                               cells and                    
                                                             Acute                                                   responses\                                                 blood vessels\               
                                                             appendicitis\                                           Viral invasion of                                          \                            
                                                             Intussusception\                                        cells and                                                  Appendia and                 
                                                             Subacute                                                secondary                                                  lymph nodes\                 
                                                             thyroiditis\                                            inflammatory                                               Intestinal                   
                                                             Sarcoma in                                              responses\                                                 lymph nodes\                 
                                                             hamsters                                                Viral invasion of                                          Thyroid\                     
                                                                                                                     mucosa cells\                                              Muscle cells                 
                                                                                                                     Viral invasion of                                                                       
                                                                                                                     lymph nodes\                                                                            
                                                                                                                     Viral invasion of                                                                       
                                                                                                                     parenchyma cells\                                                                       
                                                                                                                     Sarcoma in                                                                              
                                                                                                                     hamsters                                                                                

  Hepatitis                           \>2                    Infectious                                              Invasion of                                                Liver\                       
                                                             hepatitis\                                              parenchyma cells\                                          Liver\                       
                                                             Serum hepatitis\                                        Invasion of                                                Frontal lobe                 
                                                             Down's Syndrome                                         parenchyma cells\                                          of brain,                    
                                                                                                                     Invasion of cells                                          muscle, bones                
  ------------- -------------- ------ ----- --- ------------ ------------------ ---------------------- ------------- ----------------- ------------------- -------------------- -------------- ------------- ----------------

^4^ Pleuritis type of pain with fever

Source: Taylor, 1974; Beneson, 1981.

[]{#__RefHeading___Toc450037297 .anchor}*Table 2-3. Waterborne Diseases
from Parasites*

  ------------------ -------------------- -----------------------------------------
  **Causative        **Disease**          **Symptoms**
  Agent**                                 

  *Ascario           Ascariasis           Vomiting, live worms in feces
  lumbricoides*\                          
  (round worm)                            

  *Cryptosporidium   Cryptosporidiosis    Acute diarrhea, abdominal pain, vomiting,
  muris* and                              and low-grade fever. Can be
  *parvum*                                life-threatening in immunodeficient
                                          patients

  *Entamoeba         Amebiasis            Diarrhea alternating with constipation,
  histolytica*                            chronic dysentery with mucus and blood

  *Giardia lamblia*  Giardiasis           Intermittent diarrhea

  *Naegleria         Amoebic              Death
  gruberi*           meningoecephalitis   

  *Schistosoma       Schistosomiasis      Liver and bladder infection
  mansoni*                                

  *Taenia saginata*\ Taeniasis            Abdominal pain, digestive disturbances,
  (beef tapeworm)                         loss of weight
  ------------------ -------------------- -----------------------------------------

Source: Geldreich, 1972; Beneson, 1981.

#### Viruses

Viruses are microorganisms composed of the genetic material
deoxyribonucleic acid (DNA) or ribonucleic acid (RNA) and a protective
protein coat (either single, double, or partially double stranded). All
viruses are obligate parasites, unable to carry out any form of
metabolism and are completely dependent upon host cells for replication.
Viruses are typically 0.01 to 0.1 μm in size and are very species
specific with respect to infection, typically attacking only one type of
host. Although the principal modes of transmission for the hepatitis B
virus and poliovirus are through food, personal contact, or exchange of
body fluids, these viruses can be transmitted through potable water.
Some viruses, such as the retroviruses (including the HIV group), appear
to be too fragile for water transmission to be a significant danger to
public health (Riggs, 1989).

#### Protozoa

Protozoa are single-cell eucaryotic microorganisms without cell walls
that utilize bacteria and other organisms for food. Most protozoa are
free-living in nature and can be encountered in water; however, several
species are parasitic and live on or in host organisms. Host organisms
can vary from primitive organisms such as algae to highly complex
organisms such as human beings. Several species of protozoa known to
utilize human beings as hosts are shown in Table 2-5.

[]{#__RefHeading___Toc450037298 .anchor}Table 2-4. Attributes of the
Three Waterborne Pathogens of Concern in Water Treatment

  -------------- ----------- -------------- -------------- ---------------- ----------------
  **Organism**   **Size\     **Mobility**   **Point(s) of  **Resistance to  **Removal by
                 (µm)**                     Origin**       Disinfection**   Sedimentation,
                                                                            Coagulation, and
                                                                            Filtration**

  Bacteria       0.1--10     Motile,        Humans and     Type specific -  Good, 2 to 3-log
                             Nonmotile      animals,       bacterial spores removal
                                            water, and     typically have   
                                            contaminated   the highest      
                                            food           resistance       
                                                           whereas          
                                                           vegetative       
                                                           bacteria have    
                                                           the lowest       
                                                           resistance       

  Viruses        0.01--0.1   Nonmotile      Humans and     Generally more   Poor, 1 to 3-log
                                            animals,       resistant than   removal
                                            polluted       vegetative       
                                            water, and     bacteria         
                                            contaminated                    
                                            food                            

  Protozoa       1--20       Motile,        Humans and     More resistant   Good, 2 to 3-log
                             Nonmotile      animals,       than viruses or  removal
                                            sewage,        vegetative       
                                            decaying       bacteria         
                                            vegetation,                     
                                            and water                       
  -------------- ----------- -------------- -------------- ---------------- ----------------

[]{#__RefHeading___Toc450037299 .anchor}Table 2-5. Human Parasitic
Protozoans

  ------------------------------------------------------------------------------------------
  **Protozoan**      **Host(s)**   **Disease**           **Transmission**   **Occurrence**
  ------------------ ------------- --------------------- ------------------ ----------------
  *Acanathamoeba     Fresh water,  Amoebic               Gains entry        North America
  castellannii*      sewage,       meningoencephalitis   through abrasions, 
                     humans, and                         ulcers, and as     
                     soil                                secondary invader  
                                                         during other       
                                                         infections         

  *Balantidium coli* Pigs, humans  Balantidiasis         Contaminated water Micronesia has
                                   (dysentery)                              been the only
                                                                            known site of an
                                                                            outbreak

  *Cryptosporidium   Animals,      Cryptosporidiosis     Person-to-person   Canada, England,
  parvum*            humans                              or                 and the United
                                                         animal-to-person   States
                                                         contact, ingestion 
                                                         of fecally         
                                                         contaminated water 
                                                         or food, or        
                                                         contact with       
                                                         fecally            
                                                         contaminated       
                                                         environmental      
                                                         surfaces.          

  *Entamoeba         Humans        Amoebic dysentery     Contaminated water Last United
  histolytica*                                                              States outbreak,
                                                                            1953

  *Giardia lamblia*  Animals,      Giardiasis            Contaminated water Mexico, United
                     humans        (gastroenteritis)                        States, USSR

  *Naegleria         Soil, water,  Primary amoebic       Nasal inhalation   North America
  fowleri*           humans and    meningoencephalitis   with subsequent    
                     decaying                            penetration of     
                     vegetation                          nasopharynx;       
                                                         exposure from      
                                                         swimming in        
                                                         freshwater lakes   
  ------------------------------------------------------------------------------------------

Source: Montgomery, 1985; AWWA, 1995.

### Recent Waterborne Outbreaks

Within the past 40 years, several pathogenic agents never before
associated with documented waterborne outbreaks have appeared in the
United States. Enteropathogenic *E. coli* and *Giardia lamblia* were
first identified to be the etiological agent responsible for waterborne
outbreaks in the 1960s. The first recorded *Cryptosporidium* infection
in humans occurred in the mid-1970s. Also during that time was the first
recorded outbreak of pneumonia caused by *Legionella pneumophila*
(Centers for Disease Control, 1989; Witherell et al., 1988). Recently,
there have been numerous documented waterborne disease outbreaks that
have been caused by *E. coli, Giardia lamblia, Cryptosporidium,* and
*Legionella pneumophila.*

#### E. coli

The first documented case of waterborne disease outbreaks in the United
States associated with enteropathogenic *E. coli* occurred in the
1960s*.* Various serotypes of *E. coli* have been implicated as the
etiological agent responsible for disease in newborn infants, usually
the result of cross contamination in nurseries. Now, there have been
several well-documented outbreaks of *E. coli* (serotypes 0111:B4 and
0124:B27) associated with adult waterborne disease (AWWA, 1990, and
Craun, 1981). In 1975, the etiologic agent of a large outbreak at Crater
Lake National Park was *E. coli* serotype 06:H16 (Craun, 1981).

#### Giardia lamblia

Similar to *E. coli*, *Giardia lamblia* was first identified in the
1960s to be associated with waterborne outbreaks in the United States.
*Giardia lamblia* is a flagellated protozoan that is responsible for
Giardiasis, a disease that can range from being mildly to extremely
debilitating. *Giardia* is currently one of the most commonly identified
pathogens responsible for waterborne disease outbreaks. The life cycle
of *Giardia* includes a cyst stage when the organism remains dormant and
is extremely resilient (i.e., the cyst can survive some extreme
environmental conditions). Once ingested by a warm-blooded animal, the
life cycle of *Giardia* continues with excystation. The cysts are
relatively large (8-14 μm) and can be removed effectively by filtration
using diatomaceous earth, granular media, or membranes.

Giardiasis can be acquired by ingesting viable cysts from food or water
or by direct contact with fecal material. In addition to humans, wild
and domestic animals have been implicated as hosts. Between 1972 and
1981, 50 waterborne outbreaks of Giardiasis occurred with about 20,000
reported cases (Craun and Jakubowski, 1986). Currently, no simple and
reliable method exists to assay *Giardia* cysts in water samples.
Microscopic methods for detection and enumeration are tedious and
require examiner skill and patience. *Giardia* cysts are relatively
resistant to chlorine, especially at higher pH and low temperatures.

#### Cryptosporidium 

*Cryptosporidium* is a protozoan similar to *Giardia*. It forms
resilient oocysts as part of its life cycle. The oocysts are smaller
than *Giardia* cysts, typically about 4-6 μm in diameter. These oocysts
can survive under adverse conditions until ingested by a warm-blooded
animal and then continue with excystation.

Due to the increase in the number of outbreaks of Cryptosporidiosis, a
tremendous amount of research has focused on *Cryptosporidium* within
the last 10 years. Medical interest has increased because of its
occurrence as a life-threatening infection to individuals with depressed
immune systems. As previously mentioned, in 1993, the largest documented
waterborne disease outbreak in United States history occurred in
Milwaukee and was determined to be caused by *Cryptosporidium*. An
estimated 403,000 people became ill, 4,400 people were hospitalized, and
100 people died. The outbreak was associated with a deterioration in raw
water quality and a simultaneous decrease in effectiveness of the
coagulation-filtration process, which led to an increase in the
turbidity of treated water and inadequate removal of *Cryptosporidium*
oocysts.

#### Legionella pneumophila

An outbreak of pneumonia occurred in 1976 at the annual convention of
the Pennsylvania American Legion. A total of 221 people were affected by
the outbreak, and 35 of those afflicted died. The cause of the pneumonia
was not determined immediately despite an intense investigation by the
Centers for Disease Control. Six months after the incident,
microbiologists were able to isolate a bacterium from the autopsy lung
tissue of one of the Legionnaires. The bacterium responsible to the
outbreak was found to be distinct from other known bacterium and was
named *Legionella pneumophila* (Witherell et al., 1988)*.* Following the
discovery of this organism, other *Legionella-*like organisms were
discovered. Altogether, 26 species of *Legionella* have been identified,
and seven are etiologic agents for Legionnaires' disease (AWWA, 1990).

Legionnaires' disease does not appear to be transferred
person-to-person. Epidemiological studies have shown that the disease
enters the body through the respiratory system. *Legionella* can be
inhaled in water particles less than 5μm in size from facilities such as
cooling towers, hospital hot water systems, and recreational whirlpools
(Witherell et al., 1988).

### Mechanism of Pathogen Inactivation

The three primary mechanisms of pathogen inactivation are to:

-   Destroy or impair cellular structural organization by attacking
    major cell constituents, such as destroying the cell wall or
    impairing the functions of semi-permeable membranes;

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-   Interfere with energy-yielding metabolism through enzyme substrates
    in combination with prosthetic groups of enzymes, thus rendering the
    enzymes non-functional; and

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-   Interfere with biosynthesis and growth by preventing synthesis of
    normal proteins, nucleic acids, coenzymes, or the cell wall.

Depending on the disinfectant and microorganism type, combinations of
these mechanisms can also be responsible for pathogen inactivation. In
water treatment, it is believed that the primary factors controlling
disinfection efficiency are: (1) the ability of the disinfectant to
oxidize or rupture the cell wall; and (2) the ability of the
disinfectant to diffuse into the cell and interfere with cellular
activity (Montgomery, 1985).

## Other Uses of Disinfectants in Water Treatment

Disinfectants are used for more than just disinfection in drinking water
treatment. While inactivation of pathogenic organisms is a primary
function, disinfectants are also used oxidants in drinking water
treatment for several other functions:

-   Minimization of DBP formation;

-   Control of nuisance Asiatic clams and zebra mussels;

-   Oxidation of iron and manganese;

-   Prevention of regrowth in the distribution system and maintenance of
    biological stability;

-   Removal of taste and odors through chemical oxidation;

-   Improvement of coagulation and filtration efficiency;

-   Prevention of algal growth in sedimentation basins and filters;

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-   Removal of color.

A brief discussion of these additional oxidant uses follows.

### Minimization of DBP Formation

Strong oxidants may play a role in disinfection and DBP control
strategies in water treatment. Several strong oxidants, including
potassium permanganate and ozone, may be used to control DBP precursors.

Potassium permanganate can be used to oxidize organic precursors at the
head of the treatment plant, thus minimizing the formation of byproducts
at the downstream disinfection stage of the plant. The use of potassium
permanganate as an oxidant and disinfectant is discussed in Chapter 5 of
this guidance manual.

The use of ozone for oxidation of DBP precursors is currently being
studied. Early work has shown that the effects of ozonation, prior to
chlorination, were highly site-specific and unpredictable. The key
variables that seem to determine the effect of ozone are dose, pH,
alkalinity, and the nature of the organic material. Ozone has been shown
to be effective for DBP precursor reduction at low pHs. However, at
higher pHs (i.e., above 7.5), ozone may actually increase the amount of
chlorination byproduct precursors. The use of ozone as an oxidant and
disinfectant is addressed in detail in Chapter 3 of this document.

### Control of Nuisance Asiatic Clams and Zebra Mussels

The Asiatic clam (*Corbicula fluminea)* was introduced to the United
States from Southeast Asia in 1938 and now inhabits almost every major
river system south of 40° latitude (Britton and Morton, 1982; Counts,
1986). Asiatic clams have been found in the Trinity River, TX; the Ohio
River at Evansville, IN; New River at Narrows and Glen Lyn, VA; and the
Catawba River in Rock Hill, SC (Belanger et al., 1991; Cameron et al.,
1989a; Matisoff et al., 1996). This animal has invaded many water
utilities, clogging source water transmission systems and valves,
screens, and meters; damaging centrifugal pumps; and causing taste and
odor problems (Sinclair, 1964; Evans et al., 1979; Smith, 1979).

Cameron et al. (1989a) investigated the effectiveness of several
oxidants to control the Asiatic clam in both the juvenile and adult
phases. As expected, the adult clam was found to be much more resistant
to oxidants than the juvenile form. In many cases, the traditional
method of control, free chlorination, cannot be used because of the
formation of excessive amounts of THMs. As shown in Table 2-6, Cameron
et al. (1989a) compared the effectiveness of four oxidants for
controlling the juvenile Asiatic clam in terms of the LT50 (time
required for 50 percent mortality). Monochloramine was found to be the
best for controlling the juvenile clams without forming THMs. Further
research showed that the effectiveness of monochloramine increased
greatly as the temperature increased (Cameron et al., 1989b). Note that
the temperatures in this study reflect conditions in the Lynchburg
Reservoir, Houston, Texas. Clams can tolerate temperatures between 2 and
35°C (Cameron et al. 1989a).

[]{#__RefHeading___Toc450037300 .anchor}Table 2-6. The Effects of
Various Oxidants on Mortality of the\
Asiatic Clam (*Corbicula fluminea*)

  ---------------- ------------- ---------------- ----------- ----------- -----------
  **Chemical**     **Residual\   **Temperature\   **pH**      **Life      **LT50\
                   (mg/L)**      (°C)**                       Stage**     (days)**

  Free chlorine    0.5\          23\              8.0\        A\          8.7\
                   4.8\          21\              7.9\        A\          5.9\
                   4.7           16               7.8         J           4.8

  Potassium        1.1\          17\              7.6\        J\          7.9\
  Permanganate     4.8           17               7.6         J           8.6

  Monochloramine   2.6\          28\              7.9\        J\          0.6\
                   10.7          17               7.9         J           0.5

  Chlorine dioxide 1.2\          24\              6.9\        J\          0.7\
                   4.7           22               6.6         J           0.6
  ---------------- ------------- ---------------- ----------- ----------- -----------

> A=Adult; J=Juvenile\
> Source: Cameron et al., 1989a.

In a similar study, Belanger et al. (1991) studied the biocidal
potential of total residual chlorine, monochloramine, monochloramine
plus excess ammonia, bromine, and copper for controlling the Asiatic
clam. Belanger et al. (1991) showed that monochloramine with excess
ammonia was the most effective for controlling the clams at 30°C.
Chlorination at 0.25 to 0.40 mg/L total residual chlorine at 20 to 25°C
controlled clams of all sizes (LT50 below 28 days) but had minimal
effect at 12 to 15°C (as low as zero mortality). As in other studies,
the toxicity of all the biocides was highly dependent on temperature and
clam size.

The zebra mussel (*Dreissena polymorpha*) is a recent addition to the
fauna of the Great Lakes. It was first found in Lake St. Clair in 1988,
though it is believed that this native of the Black and Caspian seas,
was brought over from Europe in ballast water around 1985 (Herbert et
al.*,* 1989). The zebra mussel population in the Great Lakes has
expanded very rapidly, both in size and geographical distribution
(Roberts, 1990). Lang (1994) reported that zebra mussels have been found
in the Ohio River, Cumberland River, Arkansas River, Tennessee River,
and the Mississippi River south to New Orleans.

Klerks and Fraleigh (1991) evaluated the effectiveness of hypochlorite,
permanganate, and hydrogen peroxide with iron for their effectiveness
controlling adult zebra mussels. Both continuous and intermittent 28-day
static renewal tests were conducted to determine the impact of
intermittent dosing. Intermittent treatment proved to be much less
effective than continuous dosing.

The hydrogen peroxide-iron combination (1--5 mg/L with 25 percent iron)
was less effective in controlling the zebra mussel than either
permanganate or hypochlorite. Permanganate (0.5--2.5 mg KMnO~4~/L) was
usually less effective than hypochlorite (0.5--10 mg Cl~2~/L).

Van Benschoten et al. (1995) developed a kinetic model to predict the
rate of mortality of the zebra mussel in response to chlorine. The model
shows the relationship between chlorine residual and temperature on the
exposure time required to achieve 50 and 95 percent mortality. Data were
collected for chlorine residuals between 0.5 and 3.0 mg Cl~2~/L and
temperatures from 0.3 to 24°C. The results show a strong dependence on
temperature and required contact times ranging from two days to more
than a month, depending on environmental factors and mortality required.

Brady et al. (1996) compared the efficiency of chlorine to control
growth of zebra mussel and quagga mussel (*Dreissena bugensis*). The
quagga mussel is a newly identified mollusk within the Great Lakes that
is similar in appearance to the zebra mussel. Full-scale chlorination
treatment found a significantly higher mortality for the quagga mussel.
The required contact time for 100 percent mortality for quagga and zebra
mussels was 23 days and 37 days, respectively, suggesting that
chlorination programs designed to control zebra mussels should also be
effective for controlling populations of quagga mussels.

Matisoff et al. (1996) evaluated chlorine dioxide (ClO~2~) to control
adult zebra mussels using single, intermittent, and continuous
exposures. A single 30-minute exposure to 20 mg/L chlorine dioxide or
higher concentration induced at least 50 percent mortality, while sodium
hypochlorite produced only 26 percent mortality, and permanganate and
hydrogen peroxide were totally ineffective when dosed at 30 mg/L for 30
minutes under the same conditions. These high dosages, even though only
used for a short period, may not allow application directly in water for
certain applications due to byproducts that remain in the water.
Continuous exposure to chlorine dioxide for four days was effective at
concentrations above 0.5 mg/L (LC50 = 0.35 mg/L), and 100 percent
mortality was achieved at chlorine dioxide concentrations above 1 mg/L.

These experiences all show that the dose required to induce mortality to
these nuisance organisms is extremely high, both in terms of chemical
dose and contact time. The potential impact on DBPs is significant,
especially when the water is high in organic content with a high
propensity to form THMs and other DBPs.

### Oxidation of Iron and Manganese

Iron and manganese occur frequently in ground waters but are less
problematic in surface waters. Although not harmful to human health at
the low concentrations typically found in water, these compounds can
cause staining and taste problems. These compounds are readily treated
by oxidation to produce a precipitant that is removed in subsequent
sedimentation and filtration processes.

Almost all the common oxidants except chloramines will convert ferrous
(2+) iron to the ferric (3+) state and manganese (2+) to the (4+) state,
which will precipitate as ferric hydroxide and manganese dioxide,
respectively (AWWA, 1990). The precise chemical composition of the
precipitate will depend on the nature of the water, temperature, and pH.

Table 2-7 shows that oxidant doses for iron and manganese control are
relatively low. In addition, the reactions are relatively rapid, on the
order of seconds while DBP formation occurs over hours. Therefore, with
proper dosing, residual chlorine during iron and manganese oxidation is
therefore relatively low and short lived. These factors reduce the
potential for DBP formation as a result of oxidation for iron and
manganese removal.

[]{#__RefHeading___Toc450037301 .anchor}Table 2-7. Oxidant Doses
Required for Oxidation of Iron and Manganese

  --------------------------- --------------------- ---------------------
  **Oxidant**                 **Iron (II)\          **Manganese (II)\
                              (mg/mg Fe)**          (mg/mg Mn)**

  Chlorine, Cl~2~             0.62                  0.77

  Chlorine dioxide, ClO~2~    1.21                  2.45

  Ozone, O~3~                 0.43                  0.88\*

  Oxygen, O~2~                0.14                  0.29

  Potassium permanganate,     0.94                  1.92
  KMnO~4~                                           
  --------------------------- --------------------- ---------------------

> Source: Culp/Wesner/Culp, 1986; Langlais et al., 1991.
>
> \* Optimum pH for manganese oxidation using ozone is 8-8.5 Source:
> Reckhow et al., 1991.

### Prevention of Regrowth in the Distribution System and Maintenance of Biological Stability

Biodegradable organic compounds and ammonia in treated water can cause
microbial growth in the distribution system. "Biological stability"
refers to a condition wherein the treated water quality does not enhance
biological growth in the distribution system. Biological stability can
be accomplished in several ways:

-   Removing nutrients from the water prior to distribution;

-   Maintaining a disinfectant residual in the treated water; and

-   Combining nutrient removal and disinfectant residual maintenance.

To maintain biological stability in the distribution system, the Total
Coliform Rule (TCR) requires that treated water have a residual
disinfectant of 0.2 mg/L when entering the distribution system. A
measurable disinfectant residual must be maintained in the distribution
system, or the utility must show through monitoring that the
heterotrophic plate count (HPC) remains less than 500/100 mL. A system
remains in compliance as long as 95 percent of samples meet these
criteria. Chlorine, monochloramine, and chlorine dioxide are typically
used to maintain a disinfectant residual in the distribution system.
Filtration can also be used to enhance biological stability by reducing
the nutrients in the treated water.

The level of secondary disinfectant residual maintained is low,
typically in the range of 0.1-0.3 mg/L, depending on the distribution
system and water quality. However, because the contact times in the
system are quite long, it is possible to generate significant amounts of
DBPs in the distribution system, even at low disinfectant doses.

Distribution system problems associated with the use of combined
chlorine residual (chloramines), or no residual, have been documented in
several instances. The use of combined chlorine is characterized by an
initial satisfactory phase in which chloramine residuals are easily
maintained throughout the system and bacterial counts are very low.
However, problems may develop over a period of years including increased
bacterial counts, reduced combined chlorine residual, increased taste
and odor complaints, and reduced transmission main carrying capacity.
Conversion of the system to free-chlorine residual produces an initial
increase in consumer complaints of taste and odors resulting from
oxidation of accumulated organic material. Also, it is difficult to
maintain a free-chlorine concentration at the ends of the distribution
system (AWWA, 1990).

### Removal of Taste and Odors Through Chemical Oxidation

Tastes and odors in drinking water are caused by several sources,
including microorganisms, decaying vegetation, hydrogen sulfide, and
specific compounds of municipal, industrial, or agricultural origin.
Disinfectants themselves can also create taste and odor problems. In
addition to a specific taste-and odor-causing compound, the sensory
impact is often accentuated by a combination of compounds. More
recently, significant attention has been given to tastes and odors from
specific compounds such as geosmin, 2-methylisoborneol (MIB), and
chlorinated inorganic and organic compounds (AWWARF, 1987).

Oxidation is commonly used to remove taste and odor causing compounds.
Because many of these compounds are very resistant to oxidation,
advanced oxidation processes (ozone/hydrogen peroxide, ozone/UV, etc.)
and ozone by itself are often used to address taste and odor problems.
The effectiveness of various chemicals to control taste and odors can be
site-specific. Suffet et al. (1986) found that ozone is generally the
most effective oxidant for use in taste and odor treatment. They found
ozone doses of 2.5 to 2.7 mg/L and 10 minutes of contact time (residual
0.2 mg/L) significantly reduce levels of taste and odors. Lalezary et
al. (1986) used chlorine, chlorine dioxide, ozone, and permanganate to
treat earthy-musty smelling compounds. In that study, chlorine dioxide
was found most effective, although none of the oxidants were able to
remove geosmin and MIB by more than 40 to 60 percent. Potassium
permanganate has been used in doses of 0.25 to 20 mg/L. Studies at the
Metropolitan Water District of Southern California demonstrated the
effectiveness of peroxone (ozone plus hydrogen peroxide) to remove
geosmin and MIB in water treatment (Ferguson et al., 1990; Ferguson et
al., 1991; Huck et al.*,* 1995).

Prior experiences with taste and odor treatment indicate that oxidant
doses are dependent on the source of the water and causative compounds.
In general, small doses can be effective for many taste and odor
compounds, but some of the difficult-to-treat compounds require strong
oxidants such as ozone and/or advanced oxidation processes or
alternative technologies such as granular activated carbon (GAC)
adsorption.

### Improvement of Coagulation and Filtration Efficiency

Oxidants, specifically ozone, have been reported to improve coagulation
and filtration efficiency (Gurol and Pidatella, 1983; Farvardin and
Collins, 1990; Reckhow et al., 1993; Masschelein, 1992). Others,
however, have found no improvement in effluent turbidity from oxidation
(Tobiason et al., 1992; Hiltebrand et al.*,* 1986). Prendiville (1986)
collected data from a large treatment plant showing that preozonation
was more effective than prechlorination to reduce filter effluent
turbidities. The cause of the improved coagulation is not clear, but
several possibilities have been offered (Reckhow et al.*,* 1986),
including:

-   Oxidation of organics into more polar forms;

-   Oxidation of metal ions to yield insoluble complexes such as ferric
    iron complexes; and

-   Change in the structure and size of suspended particles.

### Prevention of Algal Growth in Sedimentation Basins and Filters

Prechlorination is often used to minimize operational problems
associated with biological growth in water treatment plants (AWWA, 1990;
Culp/Wesner/Culp, 1986). Prechlorination will prevent slime formation on
filters, pipes, and tanks, and reduce potential taste and odor problems
associated with such slimes. Many sedimentation and filtration
facilities operate with a small chlorine residual to prevent growth of
algae and bacteria in the launders and on the filter surfaces. This
practice has increased in recent years as utilities take advantage of
additional contact time in the treatment units to meet disinfection
requirements under the SWTR.

### Removal of Color

Free chlorine is used for color removal. A low pH is favored. Color is
caused by humic compounds, which have a high potential for DBP
formation. The chlorine dosage and kinetics for color removal are best
determined through bench studies.

## Disinfection Byproducts and Disinfection Residuals

### Types of DBPs and Disinfection Residuals

Table 2-8 is a list, compiled by EPA, of DBPs and disinfection residuals
that may be of health concern. The table includes both the disinfectant
residuals and the specific byproducts produced by the disinfectants of
interest in drinking water treatment. These contaminants of concern are
grouped into four distinct categories and include disinfectant
residuals, inorganic byproducts, organic oxidation byproducts, and
halogenated organic byproducts. Tables 1-3 and 1-4 list the disinfection
byproducts and disinfectant residuals that are currently regulated.

[]{#__RefHeading___Toc450037302 .anchor}Table 2-8. List of Disinfection
Byproducts and Disinfection Residuals

+-------------------------------+--------------------------------------+
| **DISINFECTANT RESIDUALS**    | **HALOGENATED ORGANIC BYPRODUCTS**   |
+-------------------------------+--------------------------------------+
| Free Chlorine                 | Trihalomethanes                      |
+-------------------------------+--------------------------------------+
| Hypochlorous Acid             | Chloroform                           |
+-------------------------------+--------------------------------------+
| Hypochlorite Ion              | Bromodichloromethane                 |
+-------------------------------+--------------------------------------+
| Chloramines                   | Dibromochloromethane                 |
+-------------------------------+--------------------------------------+
| Monochloramine                | Bromoform                            |
+-------------------------------+--------------------------------------+
| Chlorine Dioxide              | Haloacetic Acids                     |
+-------------------------------+--------------------------------------+
| **INORGANIC BYPRODUCTS**      | Monochloroacetic Acid                |
+-------------------------------+--------------------------------------+
| Chlorate Ion                  | Dichloroacetic Acid                  |
+-------------------------------+--------------------------------------+
| Chlorite Ion                  | Trichloroacetic Acid                 |
+-------------------------------+--------------------------------------+
| Bromate Ion                   | Monobromoacetic Acid                 |
+-------------------------------+--------------------------------------+
| Iodate Ion                    | Dibromoacetic Acid                   |
+-------------------------------+--------------------------------------+
| Hydrogen Peroxide             | Haloacetonitriles                    |
+-------------------------------+--------------------------------------+
| Ammonia                       | Dichloroacetronitrile                |
+-------------------------------+--------------------------------------+
| **ORGANIC OXIDATION           | Bromochloroacetonitrile              |
| BYPRODUCTS**                  |                                      |
+-------------------------------+--------------------------------------+
| Aldehydes                     | Dibromoacetonitrile                  |
+-------------------------------+--------------------------------------+
| Formaldehyde                  | Trichloroacetonitrile                |
+-------------------------------+--------------------------------------+
| Acetaldehyde                  | Haloketones                          |
+-------------------------------+--------------------------------------+
| > Glyoxal                     | 1,1-Dichloropropanone                |
+-------------------------------+--------------------------------------+
| Hexanal                       | 1,1,1-Trichloropropanone             |
+-------------------------------+--------------------------------------+
| Heptanal                      | Chlorophenols                        |
+-------------------------------+--------------------------------------+
| Carboxylic Acids              | 2-Chlorophenol                       |
+-------------------------------+--------------------------------------+
| Hexanoic Acid                 | 2,4-Dichlorophenol                   |
+-------------------------------+--------------------------------------+
| Heptanoic Acid                | 2,4,6-Trichlorophenol                |
+-------------------------------+--------------------------------------+
| Oxalic Acid                   | Chloropicrin                         |
+-------------------------------+--------------------------------------+
| Assimilable Organic Carbon    | Chloral Hydrate                      |
+-------------------------------+--------------------------------------+
|                               | Cyanogen Chloride                    |
+-------------------------------+--------------------------------------+
|                               | N-Organochloramines                  |
+-------------------------------+--------------------------------------+
|                               | MX\*                                 |
+-------------------------------+--------------------------------------+

\* 3-Chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone

The production of DBPs depend on the type of disinfectant, the presence
of organic material (e.g., TOC), bromide ion, and other environmental
factors as discussed in this manual. By removing DBP precursors, the
formation of DBPs can be reduced.

The health effects of DBPs and disinfectants are generally evaluated
with epidemiological studies and/or toxicological studies using
laboratory animals. Table 2-9 indicates the cancer classifications of
both disinfectants and DBPs as of January 1999. The classification
scheme used by EPA is shown at the bottom of Table 2-9. The EPA
classification scheme for carcinogenicity weighs both animal studies and
epidemiologic studies, but places greater weight on evidence of
carcinogenicity in humans.

[]{#__RefHeading___Toc450037303 .anchor}Table 2-9. Status of Health
Information for Disinfectants and DBPs

  -----------------------------------------------------------------------
  **Contaminant**                          **Cancer\
                                           Classification^(1)^**
  ---------------------------------------- ------------------------------
  Chloroform                               B2

  Bromodichloromethane                     B2

  Dibromochloromethane                     C

  Bromoform                                B2

  Monochloroacetic Acid                    \--

  Dichloroacetic Acid                      B2

  Trichloroacetic Acid                     C

  Dichloroacetonitrile                     C

  Bromochloroacetonitrile                  \--

  Dibromoacetonitrile                      C

  Trichloroacetonitrile                    \--

  1,1-Dichloropropanone                    \--

  1,1,1-Trichloropropanone                 \--

  2-Chlorophenol                           D

  2,4-Dichlorophenol                       D

  2,4,6-Trichlorophenol                    B2

  Chloropicrin                             \--

  Chloral Hydrate                          C

  Cyanogen Chloride                        \--

  Formaldehyde                             B1^(2)^

  Chlorate                                 \--

  Chlorite                                 D

  Bromate                                  B2

  Ammonia                                  D

  Hypochlorous Acid                        \--

  Hypochlorite                             \--

  Monochloramine                           \--

  Chlorine Dioxide                         D
  -----------------------------------------------------------------------

(1) The scheme for categorizing chemicals according to their
    carcinogenic potential is as follows:\*

+-------------------------+--------------------------------------------+
| Group A:\               | Sufficient evidence in epidemiologic       |
| Human Carcinogen        | studies to support casual association      |
|                         | between exposure and cancer.               |
+-------------------------+--------------------------------------------+
| Group B:\               | Limited evidence in epidemiologic studies  |
| Probable Human          | (Group B1) and/or sufficient evidence from |
| Carcinogen              | animal studies (Group B2)                  |
+-------------------------+--------------------------------------------+
| Group C:\               | Limited evidence from animal studies and   |
| Possible Human          | inadequate or no data in humans            |
| Carcinogen              |                                            |
+-------------------------+--------------------------------------------+
| Group D:\               | Inadequate or no human and animal evidence |
| Not Classifiable        | of carcinogenicity                         |
+-------------------------+--------------------------------------------+
| Group E:\               | No evidence of carcinogenicity in at least |
| No Evidence of          | two adequate animal tests in different     |
| Carcinogenicity for     | species or in adequate epidemiologic and   |
| Humans                  | animal studies.                            |
+-------------------------+--------------------------------------------+
| \* EPA is in the        |                                            |
| process of revising the |                                            |
| Cancer Guidelines       |                                            |
|                         |                                            |
| Source: USEPA, 1996     |                                            |
+-------------------------+--------------------------------------------+

^(2)^ Based on inhalation exposure.

### Disinfection Byproduct Formation

Halogenated organic byproducts are formed when natural organic matter
(NOM) reacts with free chlorine or free bromine. Free chlorine can be
introduced to water directly as a primary or secondary disinfectant,
with chlorine dioxide, or with chloramines. Free bromine results from
the oxidation of the bromide ion in source water. Factors affecting
formation of halogenated DBPs include type and concentration of natural
organic matter, oxidant type and dose, time, bromide ion concentration,
pH, organic nitrogen concentration, and temperature. Organic nitrogen
significantly influences the formation of nitrogen containing DBPs such
as the haloacetonitriles, halopicrins, and cyanogen halides (Reckhow et
al., 1990; Hoigné and Bader, 1988). The parameter TOX represents the
concentration of total organic halides in a water sample (calculated as
chloride). In general, less than 50 percent of the TOX content has been
identified, despite evidence that several of these unknown halogenated
byproducts of water chlorination may be harmful to humans (Singer and
Chang, 1989).

Non-halogenated DBPs are also formed when strong oxidants react with
organic compounds found in water. Ozone and peroxone oxidation of
organics leads to the production of aldehydes, aldo- and keto-acids,
organic acids, and, when bromide ion is present, brominated organics
(Singer, 1992). Many of the oxidation byproducts are biodegradable and
appear as biodegradable dissolved organic carbon (BDOC) and assimilable
organic carbon (AOC) in treated water.

Bromide ion plays a key role in DBP formation. Ozone or free chlorine
oxidizes bromide ion to hypobromate ion/hypobromous acid, which
subsequently forms brominated DBPs. Brominated organic byproducts
include compounds such as bromoform, brominated acetic acids and
acetonitriles, bromopicrin, and cyanogen bromide. Only about one third
of the bromide ions incorporated into byproducts has been identified.

####  Disinfection Byproduct Precursors

Numerous researchers have documented that NOM is the principal precursor
of organic DBP formation (Stevens et al., 1976; Babcock and Singer 1979;
Christman et al., 1983). Chlorine reacts with NOM to produce a variety
of DBPs, including THMs, haloacetic acids (HAAs), and others. Ozone
reacts with NOM to produce aldehydes, organic acids, and aldo- and
keto-acids; many of these are produced by chlorine as well (Singer and
Harrington, 1993).

Natural waters contain mixtures of both humic and nonhumic organic
substances. NOM can be subdivided into a hydrophobic fraction composed
of primarily humic material, and a hydrophilic fraction composed of
primarily fulvic material.

The type and concentration of NOM are often assessed using surrogate
measures. Although surrogate parameters have limitations, they are used
because they may be measured more easily, rapidly, and inexpensively
than the parameter of interest, often allowing on-line monitoring of the
operation and performance of water treatment plants. Surrogates used to
assess NOM include:

-   Total and dissolved organic carbon (TOC and DOC);

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-   Specific ultraviolet light absorbance (SUVA), which is the
    absorbance at 254 nm wavelength (UV-254) divided by DOC (SUVA =
    (UV-254/DOC)\*100, in L/mg-m);

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```
-   THM formation potential (THMFP) \-- a test measuring the quantity of
    THMs formed with a high dosage of free chlorine and a long reaction
    time; and

```{=html}
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```
-   TTHM Simulated Distribution System (SDS) \-- a test to predict the
    TTHM concentration at some selected point in a given distribution
    system, where the conditions of the chlorination test simulate the
    distribution system at the point desired.

On average, about 90 percent of the TOC is dissolved. DOC is defined as
the TOC able to pass through a 0.45 μm filter. UV absorbance is a good
technique for assessing the presence of DOC because DOC primarily
consists of humic substances, which contain aromatic structures that
absorb light in the UV spectrum. Oxidation of DOC reduces the UV
absorbance of the water due to oxidation of some of the organic bonds
that absorb UV absorbance. Complete mineralization of organic compounds
to carbon dioxide usually does not occur under water treatment
conditions; therefore, the overall TOC concentration usually is
constant.

DBP concentrations vary seasonally and are typically greatest in the
summer and early fall for several reasons:

-   The rate of DBP formation increases with increasing temperature
    (Singer et al., 1992);

```{=html}
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```
-   The nature of organic DBP precursors varies with season (Singer et
    al., 1992); and

```{=html}
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```
-   Due to warmer temperatures, chlorine demand may be greater during
    summer months requiring higher dosages to maintain disinfection.

If the bromide ion is present in source waters, it can be oxidized to
hypobromous acid that can react with NOM to form brominated DBPs, such
as bromoform. Furthermore, under certain conditions, ozone may react
with the hypobromite ion (OBr^-^) to form bromate ion (BrO^-^~3~).

The ratio of bromide ion to the chlorine dose affects THM formation and
bromine substitution of chlorine. Increasing the bromide ion to chlorine
dose ratio shifts the speciation of THMs to produce more brominated
forms (Krasner et al., 1989; Black et al., 1996). In the Krasner et al.
study, the chlorine dose was roughly proportional to TOC concentration.
As TOC was removed through the treatment train, the chlorine dose
decreased and TTHM formation declined. However, at the same time, the
bromide ion to chlorine dose increased, thereby shifting TTHM
concentrations to the more brominated THMs. Therefore, improving the
removal of NOM prior to chlorination can shift the speciation of
halogenated byproducts toward more brominated forms.

Chloropicrin is produced by the chlorination of humic materials in the
presence of nitrate ion (Duguet et al., 1985; Thibaud et al., 1987).
Thibaud et al. (1988) chlorinated humic compounds in the presence of
bromide ion to demonstrate the formation of brominated analogs to
chloropicrin.

#### Impacts of pH on DBP Formation

The pH of water being chlorinated has an impact on the formation of
halogenated byproducts as shown in Table 2-10 (Reckhow and Singer, 1985;
Stevens et al., 1989). THM formation increases with increasing pH.
Trichloroacetic acid, dichloroacetonitrile, and trichloropropanone
formation decrease with increased pH. Overall TOX formation decreases
with increasing pH.

Based on chlorination studies of humic material in model systems, high
pH tends to favor chloroform formation over the formation of
trichloroacetic acid and other organic halides. Accordingly, water
treatment plants practicing precipitative softening at pH values greater
than 9.5 to 10 are likely to have a higher fraction of TOX attributable
to THMs than plants treating surface waters by conventional treatment in
pH ranges of 6 to 8 (Singer and Chang, 1989).

Since the application of chlorine dioxide and chloramines may introduce
free chlorine into water, chlorination byproducts that may be formed
would be influenced by pH as discussed above. Ozone application to
bromide ion containing waters at high pH favors the formation of bromate
ion, while application at low pH favors the formation of brominated
organic byproducts. See discussion under individual disinfectants for a
more detailed discussion on pH impacts on DBP formation.

The pH also impacts enhanced coagulation (i.e., for ESWTR compliance)
and Lead and Copper Rule Compliance. These issues are addressed in EPA's
*Microbial and Disinfection Byproduct Simultaneous Compliance Guidance
Manual* (expected to be available in 1999).

#### Organic Oxidation Byproducts

Organic oxidation byproducts are formed by reactions between NOM and all
oxidizing agents added during drinking water treatment. Some of these
byproducts are halogenated, as discussed in the previous section, while
others are not. The types and concentrations of organic oxidation
byproducts produced depend on the type and dosage of the oxidant being
used, chemical characteristics and concentration of the NOM being
oxidized, and other factors such as the pH and temperature.

Specific chemical byproducts belonging to the classification of
halogenated organic oxidation products are listed in Table 2-10. As
presented in Table 2-10, the formation of DBPs is pH dependent.
Comparisons in the table are made to the formation of TTHMs at a pH of
7.0. AOC is not a specific organic contaminant, but a generally used
surrogate measure of bacterial regrowth potential in distribution
systems. AOC is comprised of many chemical species, including the
aldehydes and carboxylic acids listed in Table 2-8. AOC formation
studies, primarily performed in the Netherlands, have shown that both
ozonation and chlorination can increase concentrations of AOC. This
increase in AOC concentration is believed to be the result of oxidizing
high molecular weight organics to smaller and more readily
bioassimilable molecules. Because AOC is not a specific chemical
contaminant, no specific health effects are attributable to AOC.

[]{#__RefHeading___Toc450037304 .anchor}Table 2-10. Conditions of
Formation of DBPs

  -------------------------- ----------------- ----------------- -----------------
                             **Conditions of                     
                             Formation**                         

  **By-product**             **Chlorination at **Chlorination at **Chlorination at
                             pH 5.0**          pH 7.0**          pH 9.4**

  Total Trihalomethanes      Lower formation                     Higher formation

  Trichloroacetic Acid       Similar formation Similar formation Lower formation
                             to that at pH 7.0 to that at pH 5.0 

  Dichloroacetic Acid        Similar formation Similar formation Similar formation
                             to that at pH 5.0 to that at pH 5.0 to that at pH 5.0
                             and 9.4 - perhaps and 9.4- perhaps  and 7.0 - perhaps
                             slightly higher   slightly higher   slightly higher
                             at pH 7.0         at pH 7.0         at pH 7.0

  Monochloroacetic Acid      At concentrations At concentrations At concentrations
                             \<5 μg/L, trends  \<5 μg/L, trends  \<5 μg/L, trends
                             not discernible   not discernible   not discernible

  Dibromoacetic Acid         At concentrations At concentrations At concentrations
                             \<1 μg/L, trends  \<1 μg/L, trends  \<1 μg/L, trends
                             not discernible   not discernible   not discernible

  Chloral Hydrate            Similar formation Similar formation Forms within 4
                             to that at pH 7.0 to that at pH 5.0 hours; decays
                                                                 over time to \<5
                                                                 μg/L

  Chloropicrin               At concentrations At concentrations At concentrations
                             \<1 μg/L, trends  \<1 μg/L, trends  \<1 μg/L, trends
                             not discernible   not discernible   not discernible

  Dichloroacetonitrile       Higher formation  Forms within 4    Concentrations
                                               hours; decays     \<2 μg/L, trends
                                               over time to \<5  not discernible
                                               μg/L              

  Bromochloroacetonitrile    At concentrations At concentrations At concentrations
                             \<2 μg/L, trends  \<2 μg/L, trends  \<2 μg/L, trends
                             not discernible   not discernible   not discernible

  Dibromoacetonitrile        At concentrations At concentrations At concentrations
                             \<.5 μg/L, trends \<.5 μg/L, trends \<.5 μg/L, trends
                             not discernible   not discernible   not discernible

  Trichloroacetonitrile      Not detected      Not detected      Not detected

  1,1,1-Trichloropropanone   Higher formation  At concentrations Not detected
                                               \<2 μg/L, trends  
                                               not discernible   
  -------------------------- ----------------- ----------------- -----------------

Source: Stevens et al., 1989.

#### Inorganic Byproducts and Disinfectants

Table 2-11 shows some of the inorganic DBPs that are produced or remain
as residual during disinfection. As discussed earlier, bromide ion
reacts with strong oxidants to form bromate ion and other organic DBPs.
Chlorine dioxide and chloramines leave residuals that are of concern for
health considerations, as well as for taste and odor. The significance
of these compounds is discussed further in subsequent chapters.

[]{#__RefHeading___Toc450037305 .anchor}Table 2-11. Inorganic DBPs
Produced During Disinfection

  ------------------ -----------------------------------------------------
  **Disinfectant**   **Inorganic Byproduct or Disinfectant Residual
                     Discussed**

  Chlorine Dioxide   Chlorine Dioxide, Chlorite ion, Chlorate ion, Bromate
                     ion (in presence of light)

  Ozone              Bromate ion, Hydrogen Peroxide

  Chloramination     Monochloramine, Dichloramine, Trichloramine, Ammonia,
                     Cyanogen Chloride
  ------------------ -----------------------------------------------------

### DBP Control Strategies

In 1983, the EPA identified technologies, treatment techniques, and
plant modifications that community water systems could use to comply
with the maximum contaminant level for TTHMs. The principal treatment
modifications involved moving the point of chlorination downstream in
the water treatment plant, improving the coagulation process to enhance
the removal of DBP precursors, and using chloramines to supplement or
replace the use of free chlorine (Singer, 1993). Moving the point of
chlorination downstream in the treatment train often is very effective
in reducing DBP formation, because it allows the NOM precursor
concentration to be reduced during treatment prior to chlorine addition.
Replacing prechlorination by preoxidation with an alternate disinfectant
that produces less DBPs is another option for reducing formation of
chlorinated byproducts.

Other options to control the formation of DBPs include; source water
quality control, DBP precursor removal, and disinfection strategy
selection. An overview of each is provided below.

#### Source Water Quality Control

Source water control strategies involve managing the source water to
lower the concentrations of NOM and bromide ion in the source water.
Research has shown that algal growth leads to the production of DBP
precursors (Oliver and Shindler, 1980; Wachter and Andelman, 1984;
Karimi and Singer, 1991). Therefore, nutrient and algal management is
one method of controlling DBP formation potential of source waters.
Control of bromide ion in source waters may be accomplished by
preventing brine or salt water intrusion into the water source.

#### DBP Precursor Removal

Raw water can include DBP precursors in both dissolved and particulate
forms. For the dissolved precursors to be removed in conventional
treatment, they must be converted to particulate form for subsequent
removal during settling and filtering. The THM formation potential
generally decreases by about 50 percent through conventional coagulation
and settling, indicating the importance of moving the point of chlorine
application after coagulation and settling (and even filtration) to
control TOX as well as TTHM formation (Singer and Chang, 1989).
Conventional systems can lower the DBP formation potential of water
prior to disinfection by further removing precursors with enhanced
coagulation, GAC adsorption, or membrane filtration prior to
disinfection. Precursor removal efficiencies are site-specific and vary
with different source waters and treatment techniques.

Aluminum (alum) and iron (ferric) salts can remove variable amounts of
NOM. For alum, the optimal pH for NOM removal is in the range of 5.5 to
6.0. The addition of alum decreases pH and may allow the optimal pH
range to be reached without acid addition. However, waters with very low
or very high alkalinities may require the addition of base or acid to
reach the optimal NOM coagulation pH (Singer, 1992).

GAC adsorption can be used following filtration to remove additional
NOM. For most applications, empty bed contact times in excess of 20
minutes are required, with regeneration frequencies on the order of 2 to
3 months (Singer, 1992). These long contact times and frequent
regeneration requirements make GAC an expensive treatment option. In
cases where prechlorination is practiced, the chlorine rapidly degrades
GAC. Addition of a disinfectant to the GAC bed can result in specific
reactions in which previously absorbed compounds leach into the treated
water.

Membrane filtration has been shown effective in removing DBP precursors
in some instances. In pilot studies, ultrafiltration (UF) with a
molecular weight cutoff (MWCO) of 100,000 daltons was ineffective for
controlling DBP formation. However, when little or no bromide ion was
present in source water, nanofiltration (NF) membranes with MWCOs of 400
to 800 daltons effectively controlled DBP formation (Lâiné et al.,
1993). In waters containing bromide ion, higher bromoform concentrations
were observed after chlorination of membrane permeate (compared with raw
water). This occurs as a result of filtration removing NOM while
concentrating bromide ions in the permeate thus providing a higher ratio
of bromide ions to NOM than in raw water. This reduction in chlorine
demand increases the ratio of bromide to chlorine, resulting in higher
bromoform concentrations after chlorination of NF membrane permeate
(compared with the raw water). TTHMs were lower in chlorinated permeate
than chlorinated raw water. However, due to the shift in speciation of
THMs toward more brominated forms, bromoform concentrations were
actually greater in chlorinated treated water than in chlorinated raw
water. Use of spiral-wound NF membranes (200--300 daltons) more
effectively controlled the formation of brominated THMs, but
pretreatment of the water was necessary (Lâiné et al., 1993).
Significant limitations in the use of membranes are disposal of the
waste brine generated, fouling of membranes, cost of membrane
replacement, and increasing energy cost.

The promulgated DBPR requires enhanced coagulation as an initial step
for removal of DBP precursors. In addition to meeting MCLs and MRDLs,
some water suppliers also must meet treatment requirements to control
the organic material (DBP precursors) in the raw water that combines
with disinfectant residuals to form DBPs. Systems using conventional
treatment are required to control precursors (measured as TOC) by using
enhanced coagulation or enhanced softening. A system must remove a
specified percentage of TOC (based on raw water quality) prior to the
point of continuous disinfection (Table 2-12).

Systems using ozone followed by biologically active filtration or
chlorine dioxide that meet specific criteria would be required to meet
the TOC removal requirements prior to addition of a residual
disinfectant. Systems able to reduce TOC by a specified percentage level
have met the DBPR treatment technique requirement.

[]{#__RefHeading___Toc450037306 .anchor}Table 2-12. Required Removal of
TOC by Enhanced Coagulation for Surface Water Systems^+^ Using
Conventional Treatment^++^ (percent reduction)

  ------------------------------------------------------------------------
                     **Source Water                      
                     Alkalinity (mg/L                    
                     as CaCO~3~)**                       
  ------------------ ----------------- ----------------- -----------------
  **Source Water\    **0-60**          **\>60-120**      **\>120^+++^**
  TOC (mg/L)**                                           

  \>2.0-4.0          35.0              25.0              15.0

  \>4.0-8.0          45.0              35.0              25.0

  \>8.0              50.0              40.0              30.0
  ------------------------------------------------------------------------

\+ Also applies to utilities that treat ground water under the influence
of surface water.

++ Systems meeting at least one of the conditions in 40 CFR §§
141.135(a)(1)(I)-(iv) are not required to operate with enhanced
coagulation.

+++ Systems practicing precipitative softening must meet the TOC removal
requirements in this column.

If the system does not meet the percent reduction, it must determine its
alternative minimum TOC removal level. The primacy agency approves the
alternative minimum TOC removal possible for the system on the basis of
the relationship between coagulant dose and TOC in the system based on
results of bench or pilot-scale testing. Enhanced coagulation is
determined in part as the coagulant dose where an incremental addition
of 10 mg/L of alum (or an equivalent amount of ferric salt) results in a
TOC removal below 0.3 mg/L.

#### Disinfection Strategy Selection

In addition to improving the raw or predisinfectant water quality,
alternative disinfection strategies can be used to control DBPs. These
strategies include the following:

-   Use an alternative or supplemental disinfectant or oxidant such as
    chloramines or chlorine dioxide that will produce fewer DBPs;

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-   Move the point of chlorination to reduce TTHM formation and, where
    necessary, substitute chloramines, chlorine dioxide, or potassium
    permanganate for chlorine as a preoxidant;

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```
-   Use two different disinfectants or oxidants at various points in the
    treatment plant to avoid DBP formation at locations where precursors
    are still present in high quantities;

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```
-   Use of powdered activated carbon for THM precursor or TTHM reduction
    seasonally or intermittently; and

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```
-   Maximize precursor removal.

### CT Factor

One of the most important factors for determining or predicting the
germicidal efficiency of any disinfectant is the CT factor, a version of
the Chick-Watson law (Chick, 1908; Watson, 1908). The CT factor is
defined as the product of the residual disinfectant concentration, C, in
mg/L, and the contact time, T, in minutes, that residual disinfectant is
in contact with the water.

EPA developed CT values for the inactivation of *Giardia* and viruses
under the SWTR. Table 2‑13 compares the CT values for virus inactivation
using chlorine, chlorine dioxide, ozone, chloramine, and ultraviolet
light disinfection under specified conditions. Table 2-14 shows the CT
values for inactivation of *Giardia* cyst using chlorine, chloramine,
chlorine dioxide, and ozone under specified conditions. The CT values
shown in Table 2-13 and Table 2-14 are based on water temperatures of
10°C and pH values in the range of 6 to 9. CT values for chlorine
disinfection are based on a free chlorine residual. Note that chlorine
is less effective as pH increases from 6 to 9. In addition, for a given
CT value, a low C and a high T is more effective than the reverse (i.e.,
a high C and a low T). For all disinfectants, as temperature increases,
effectiveness increases.

[]{#__RefHeading___Toc450037307 .anchor}Table 2-13. CT Values for
Inactivation of Viruses

  ------------------ ------------- ------------------ ------------- -------------
  **Disinfectant**   **Units**     **Inactivation**                 

                                   2-log              3-log         4-log

  Chlorine^1^        mg · min/L    3                  4             6

  Chloramine^2^      mg · min/L    643                1,067         1,491

  Chlorine           mg · min/L    4.2                12.8          25.1
  Dioxide^3^                                                        

  Ozone              mg · min/L    0.5                0.8           1.0

  UV                 mW · s/cm^2^  21                 36            not available
  ------------------ ------------- ------------------ ------------- -------------

CT values were obtained from AWWA, 1991.

^1^ Values are based on a temperature of 10°C, pH range of 6 to 9, and a
free chlorine residual of 0.2 to 0.5 mg/L.

^2^ Values are based on a temperature of 10°C and a pH of 8.

^3^ Values are based on a temperature of 10°C and a pH range of 6 to 9.

[]{#__RefHeading___Toc450037308 .anchor}Table 2-14. CT Values for
Inactivation of *Giardia* Cysts

  ------------------ ---------------- --------- --------- --------- --------- ---------
  **Disinfectant**   **Inactivation                                           
                     (mg · min/L)**                                           

                     0.5-log          1-log     1.5-log   2-log     2.5-log   3-log

  Chlorine^1^        17               35        52        69        87        104

  Chloramine^2^      310              615       930       1,230     1,540     1,850

  Chlorine           4                7.7       12        15        19        23
  Dioxide^3^                                                                  

  Ozone^3^           0.23             0.48      0.72      0.95      1.2       1.43
  ------------------ ---------------- --------- --------- --------- --------- ---------

CT values were obtained from AWWA, 1991.

^1^ Values are based on a free chlorine residual less than or equal to
0.4 mg/L, temperature of 10°C, and a pH of 7.

^2^ Values are based on a temperature of 10°C and a pH in the range of 6
to 9.

^3^ Values are based on a temperature of 10°C and a pH of 6 to 9.

## Pathogen Inactivation Versus DBP Formation

Table 2-15 presents a summary of disinfection parameter impacts on
pathogen inactivation and DBP formation.

[]{#__RefHeading___Toc450037309 .anchor}Table 2-15. Summary of
Disinfection Impacts

  ------------------ -------------------------- --------------------------
  **Disinfection     **Typical Impact on        **Typical Impact on DBP
  Parameter**        Pathogen Inactivation**    Formation**

  Disinfectant Type  Depends on inactivation    Depends on disinfectant
                     efficacy                   reactivity

  Disinfectant       The stronger the           The stronger the
  Strength           disinfectant, the quicker  disinfectant, the greater
                     the disinfection process.  the amount of DBPs.

  Disinfectant Dose  Increasing the             Increasing the
                     disinfectant dose          disinfectant dose
                     increases the disinfection typically increases the
                     rate.                      rate of DBP formation.

  Type of Organism   Susceptibility to          None.
                     disinfection varies        
                     according to pathogen      
                     group. In general,         
                     protozoa are more          
                     resistant to disinfectants 
                     than bacteria and viruses. 

  Contact Time       Increasing the contact     Increasing contact time
                     time decreases the         with an equivalent
                     disinfectant dose required disinfectant dose
                     for a given level of       increases the formation of
                     inactivation.              DBPs.

  pH                 pH may affect the          The impact of pH varies
                     disinfectant form and,     with DBP. See Section
                     in-turn, the efficiency of 2.3.2.3 for a brief
                     the disinfectant.          summary of relationships
                                                between pH and DBP
                                                formation.

  Temperature        Increasing the temperature Increasing temperature is
                     increases the rate of      typically associated with
                     disinfection.              faster oxidation kinetics,
                                                hence, increased DBP
                                                formation.

  Turbidity          Particles responsible for  Increased turbidity may be
                     turbidity can surround and associated with increased
                     shield pathogenic          NOM, which represents an
                     microorganisms from        increased amount of DBP
                     disinfectants.             precursors for the
                                                formation of DBPs when
                                                disinfectant is applied.

  Dissolved Organics Dissolved organics can     Increased dissolved
                     interfere with             organics will represent a
                     disinfection by creating a larger amount of DBP
                     demand and reducing the    precursor for the
                     amount of disinfectant     formation of DBPs when
                     available for pathogen     disinfectant is applied.
                     inactivation.              
  ------------------ -------------------------- --------------------------

## Disinfectant Residual Regulatory Requirements

One of the most important factors for evaluating the merits of
alternative disinfectants is their ability to maintain the microbial
quality in the water distribution system. Disinfectant residuals may
serve to protect the distribution system against regrowth (Snead et al.,
1980). The SWTR requires that filtration and disinfection must be
provided to ensure that the total treatment of the system achieves at
least a 3-log removal/inactivation of *Giardia* cysts and a 4-log
removal/inactivation of viruses. In addition, the disinfection process
must demonstrate by continuous monitoring and recording that the
disinfectant residual in the water entering the distribution system is
never less than 0.2 mg/L for more than 4 hours.

Several of the alternative disinfectants examined in this manual cannot
be used to meet the residual requirements stated in the SWTR. For
example, if either ozone or ultraviolet light disinfection are used as
the primary disinfectant, a secondary disinfectant such as chlorine or
chloramines should be utilized to obtain a residual in the distribution
system.

DBP formation continues in the distribution system due to reactions
between the residual disinfectant and organics in the water. Koch et al.
(1991) found that with a chlorine dose of 3-4 mg/L, THM and HAA
concentrations increase rapidly during the first 24 hours in the
distribution system. After the initial 48 hours, the subsequent increase
in THMs is very small. Chloral hydrate concentrations continued to
increase after the initial 24 hours, but at a reduced rate. Haloketones
actually decreased in the distribution system.

Nieminski et al. (1993) evaluated DBP formation in the simulated
distribution systems of treatment plants in Utah. Finished water
chlorine residuals ranged from 0.4 to 2.8 mg/L. Generally, THM values in
the distribution system studies increased by 50 to 100 percent (range of
30 to 200 percent) of the plant effluent value after 24-hour contact
time. The 24-hour THM concentration was essentially the same as the
7-day THM formation potential. HAA concentrations in the simulated
distribution system was about 100 percent (range of 30 to 200 percent)
of the HAA in the plant effluent. The 7-day HAA formation potential was
sometimes higher, or below the distribution system values. If chlorine
is used as a secondary disinfectant, one should therefore anticipate a
100-percent increase in the plant effluent THMs, or plan to reach the
7-day THM formation level in the distribution system.

## Summary of Current National Disinfection Practices

Most water treatment plants disinfect water prior to distribution. The
1995 Community Water Systems Survey (USEPA, 1997a) reports that 81
percent of all community water systems provide some form of treatment on
all or a portion of their water sources. The survey also found that
virtually all surface water systems provide some treatment of their
water. Of those systems reporting no treatment, 80 percent rely on
ground water as their only water source.

The most commonly used disinfectants/oxidants are chlorine, chlorine
dioxide, chloramines, ozone, and potassium permanganate. Table 2-16
shows a breakdown on the chemical usage from the survey. Note that the
table shows the percentages of systems using the particular chemical as
either disinfectant or some other role. The table shows the predominance
of chlorine in surface and ground water disinfection treatment systems
with more than 60 percent of the treatment systems using chlorine as
disinfectant/oxidant. Potassium permanganate on the other hand, is used
by many systems, but its application is primarily for oxidation, rather
than for disinfection.

Permanganate will have some beneficial impact on disinfection since it
is a strong oxidant that will reduce the chemical demand for the
ultimate disinfection chemical. Chloramine is used by some systems and
is more frequently used as a post-treatment disinfectant.

The International Ozone Association conducted a survey of ozone
facilities in the United States (IOA, 1997). The survey documented the
types of ozone facilities, size, objective of ozone application, and
year of operation. Table 2-17 summarizes the findings from the survey.
The most common use for ozone is for oxidation of iron and manganese,
and for taste and odor control. Twenty-four of the 158 ozone facilities
used GAC following ozonation. In addition to the 158 operating ozone
facilities, the survey identified 19 facilities under construction and
another 30 under design. The capacity of the systems range from less
than 25 gpm to exceeding 500 mgd. Nearly half of the operating
facilities have a capacity exceeding 1 mgd. Rice et al. (1998) found
that as of May 1998, 264 drinking water plants in the United States are
using ozone.

[]{#__RefHeading___Toc450037310 .anchor}Table 2-16. Disinfection
Practices of Water Systems that Include Some Form of Treatment

  --------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------
  **Treatment**               **Service                                                                                                                                                                                                                 
                              Population**                                                                                                                                                                                                              
  --------------------------- -------------- ------- -------- ------------- ------- ------- --------------- ------- ----------------- ------- ------------------ ------- ------------------- ----- -------------------- ---- ----------- -- ----------- --------
                              **\<100**                       **101-500**                   **501-1,000**           **1,001-3,300**           **3,301-10,000**           **10,001-50,000**         **50,001-100,000**        **Over         **Total**   
                                                                                                                                                                                                                             100,001**                  

  **Surface Water Systems**                                                                                                                                                                                                                             

  **Total Number of Systems**                218              432                           330                     845                       679                        626                       103                       104            3,337       

  **Pre-Disinfection,                                                                                                                                                                                                                                   
  Oxidation/Softening**                                                                                                                                                                                                                                 

  Chlorine                                   59.0%            73.9%                         67.3%                   66.3%                     68.8%                      58.6%                     47.5%                     57.1%          63.8%       

  Chlorine dioxide                           0                0                             0                       5.0                       4.7                        13.2                      14.2                      7.8            6.3         

  Chloramines                                4.6              0                             1.1                     2.1                       0                          2.2                       15.5                      10.8           3.1         

  Ozone                                      0                0                             0                       0                         0.3                        0                         5.4                       5.8            0.9         

  KMnO~4~                                    0                4.9                           9.6                     9.9                       15.2                       28.3                      25.9                      28.5           16.0        

  Predisinfection/oxidation                  0                0                             2.0                     2.9                       0.6                        9.2                       5.1                       4.3            3.5         

  Lime/Soda ash softening                    6.8              9.8                           20.9                    16.2                      14.3                       11.7                      3.5                       5.9            12.5        

  Recarbonation                              0                0                             0                       0                         2.1                        4.7                       0.6                       6.3            1.9         

  **Post-Disinfection**                                                                                                                                                                                                                                 

  Chlorine                    49.7 %                          51.6%                         80.6%                   62.8%                     77.9%                      71.1%                     73.8 %                    63.6 %         67.5 %      

  Chlorine dioxide            0                               0                             0                       0                         0.3                        4.9                       5.9                       11.2           1.6         

  Chloramines                 0                               0                             0                       2.9                       2.1                        15.6                      29.4                      24.2           8.1         

  Postdisinfection            0                               0                             0                       2.1                       4.0                        3.9                       1.9                       1.6            3.0         
  combinations                                                                                                                                                                                                                                          

  **Ground Water Systems**                                                                                                                                                                                                                              

  **Total Number of Systems** 9,042                  10,367                         4,443                   4,422                     2,035                      1,094                       120                        56                              31,579

  **Pre-Disinfection,                                                                                                                                                                                                                                   
  Oxidation/Softening**                                                                                                                                                                                                                                 

  Chlorine                                   64.2 %                         69.9 %          56.7 %                  73.2 %                    60.6 %                     57.4 %                    36.2 %                    38.1 %         63.9 %      

  Chlorine dioxide                           1.3                            0               0                       0                         0                          0                         3.1                       0              0.3         

  Chloramines                                0                              0               0                       0                         0                          0.6                       1.4                       0.7            0.1         

  Ozone                                      0                              0               0                       0                         0                          0                         0                         0.6            0           

  KMnO~4~                                    0                              0.9             2.2                     0.6                       5.8                        3.2                       7.0                       0              1.8         

  Predisinfection/oxidation                  0.3                            0.5             0                       0.7                       1.0                        2.6                       0                         0              0.7         

  Lime/Soda ash softening                    2.9                            2.9             2.2                     3.6                       3.5                        3.8                       5.0                       9.1            3.2         

  Recarbonation                              0                              0.5             0                       0.6                       1.4                        1.5                       2.8                       1.1            0.6         

  **Post-Disinfection**                                                                                                                                                                                                                                 

  Chlorine                                   23.0 %                         23.4%           32.5%                   28.3 %                    42.5%                      41.9 %                    54.5 %                    65.8 %         31.0 %      

  Chlorine dioxide                           0                              1.0             0                       0                         0                          0.6                       0                         0              0.4         

  Chloramines                                0                              0               0                       0                         0.1                        1.1                       3.9                       4.3            0.3         

  Postdisinfection                           0                              0               0                       0                         0.1                        0.1                       0                         0              0           
  combinations                                                                                                                                                                                                                                          
  --------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------

Source: USEPA, 1997a.

[]{#__RefHeading___Toc450037311 .anchor}Table 2-17. Ozone Application in
Water Treatment Plants in the United States

  ------------------------------- ------------------- -------------------
  **Ozone Objective**             **Number of         **% Plants**
                                  Plants**            

  THM Control                     50                  32

  Disinfection                    63                  40

  Iron/Manganese, Taste and Odor  92                  58
  Control                                             

  Total                           158                 \--
  ------------------------------- ------------------- -------------------

Source: IOA, 1997.

## Chlorine

Although chlorine is not a focus of this guidance manual, the following
section provides a brief overview of chlorine use in the water treatment
industry to compare with the alternative disinfectants discussed in this
manual. Since there is a wealth of excellent literature on chlorine's
uses and performance capabilities, summarizing this large body of
knowledge here is neither practical nor necessary (see, for example:
White, 1992; Chlorine Institute, 1996; and Connell, 1996).

One of the recent developments in chlorine disinfection is the use of
multiple and interactive disinfectants. In these applications, chlorine
is combined with a second disinfectant to achieve improved disinfection
efficiency and/or effective DBP control. A detailed discussion on
multiple disinfectants, including chlorine combinations, is provided in
Chapter 9.

As described earlier, the 1995 Community Water System Survey (USEPA,
1997a), indicated that the majority of all surface water and ground
water systems in the United States use chlorine for disinfection.

Chlorine has many attractive features that contribute to its wide use in
the industry. Four of the key attributes of chlorine are that it:

-   Effectively inactivates a wide range of pathogens commonly found in
    water;

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-   Leaves a residual in the water that is easily measured and
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-   Is economical; and

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-   Has an extensive track record of successful use in improving water
    treatment operations (despite the dangers associated with chlorine
    application and handling, specifically chlorine gas, it still
    maintains an excellent safety record).

There are, however, some concerns regarding chlorine usage that may
impact its uses such as:

-   Chlorine reacts with many naturally occurring organic and inorganic
    compounds in water to produce undesirable DBPs;

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-   Hazards associated with using chlorine, specifically chlorine gas,
    require special treatment and response programs; and

-   High chlorine doses can cause taste and odor problems.

Chlorination is used in water treatment facilities primarily for
disinfection. Because of chlorine's oxidizing powers, it has been found
to serve other useful purposes in water treatment, such as (White,
1992):

-   Taste and odor control;

-   Prevention of algal growths;

-   Maintenance of clear filter media;

-   Removal of iron and manganese;

-   Destruction of hydrogen sulfide;

-   Bleaching of certain organic colors;

-   Maintenance of distribution system water quality by controlling
    slime growth;

-   Restoration and preservation of pipeline capacity;

-   Restoration of well capacity, water main sterilization; and

-   Improved coagulation by activated silica.

### Chlorine Chemistry

Chlorine for disinfection typically is used in one of three forms:
chlorine gas, sodium hypochlorite, or calcium hypochlorite. A brief
description of the chemistry of these three chemicals is provided below.

#### Chlorine Gas

Chlorine gas hydrolyzes rapidly in water to form hypochlorous acid
(HOCl). The following equation presents the hydrolysis reaction:

*Cl*~2(g)~ + H~2~O ⇒ HO*Cl* + H^+^ *Cl*^-^ *Equation 1*

Note that the addition of chlorine gas to water reduces the pH of the
water due to the production of hydrogen ion.

Hypochlorous acid is a weak acid (pK~a~ of about 7.5), meaning it
dissociates slightly into hydrogen and hypochlorite ions as noted in
Equation 2:

*HOCl ⇔* H^+^ + O *Cl*^-^ *Equation 2*

Between a pH of 6.5 and 8.5 this dissociation is incomplete and both
HOCl and OCl^-^ species are present to some extent (White, 1992). Below
a pH of 6.5, no dissociation of HOCl occurs, while above a pH of 8.5,
complete dissociation to OCl^-^ occurs. As the germicidal effects of
HOCl is much higher than that of OCl^-^, chlorination at a lower pH is
preferred.

#### Hypochlorite

In addition to chlorine gas, chlorine is also available in hypochlorite
form as both aqueous solutions and dry solids. The most common aqueous
hypochlorite solution is sodium hypochlorite. The most common form of
dry solid hypochlorite is calcium hypochlorite (White, 1992).

**Sodium Hypochlorite.** Sodium hypochlorite is produced when chlorine
gas is dissolved in a sodium hydroxide solution. Sodium hypochlorite
solution typically contains 12.5 percent available chlorine (White,
1992). One gallon of 12.5 percent sodium hypochlorite solution typically
contains the equivalent of one pound of chlorine.

The reaction between sodium hypochlorite and water is shown in the
following reaction:

*NaOCl* + H~2~O ⇒ HO*Cl* + Na^+^ + OH^-^ *Equation 3*

Equation 3 shows that the application of sodium hypochlorite to water
produces hypochlorous acid, similar to chlorine gas hydrolysis (Equation
1). However, unlike chlorine hydrolysis, the addition of sodium
hypochlorite to water yields a hydroxyl ion that will increase the pH of
the water. In addition, excess sodium hydroxide is used to manufacture
sodium hypochlorite, which will further increase the pH of the water.

**Calcium Hypochlorite.** Calcium hypochlorite is formed from the
precipitate that results from dissolving chlorine gas in a solution of
calcium oxide (lime) and sodium hydroxide. Granular calcium hypochlorite
commercially available typically contains 65 percent available chlorine.
This means that 1.5 pounds of calcium hypochlorite contains the
equivalent of one pound of chlorine. The reaction between calcium
hypochlorite and water is shown in the following reaction:

*Ca(OCl)~2~* + 2H~2~O ⇒ 2HO*Cl* + Ca^++^ + 2OH^-^ *Equation 4*

Equation 4 shows that the application of calcium hypochlorite to water
also produces hypochlorous acid, similar to chlorine gas hydrolysis
(Equation 1). Similar to sodium hypochlorite solution, the addition of
calcium hypochlorite to water yields hydroxyl ions that will increase
the pH of the water.

### Chlorine Generation

Onsite generation of chlorine has recently become practical. These
generation systems, using only salt and electric power, can be designed
to meet disinfection and residual standards and to operate unattended at
remote sites. Considerations for chlorine generation include cost,
concentration of the brine produced, availability of raw materials, and
the reliability of the process (AWWA and ASCE, 1997).

#### Chlorine

Chlorine gas can be generated by a number of processes including the
electrolysis of alkaline brine or hydrochloric acid, the reaction
between sodium chloride and nitric acid, or the oxidation of
hydrochloric acid. About 70 percent of the chlorine produced in the
United States is manufactured from the electrolysis of salt brine and
caustic solutions in a diaphragm cell (White, 1992). Since chlorine is a
stable compound, it is typically produced off-site by a chemical
manufacturer. Once produced, chlorine is packaged as a liquefied gas
under pressure for delivery to the site in railcars, tanker trucks, or
cylinders.

#### Sodium Hypochlorite

Dilute sodium hypochlorite solutions (less than 1 percent) can be
generated electrochemically on-site from salt brine solution. Typically,
sodium hypochlorite solutions are referred to as liquid bleach or
Javelle water. Generally, the commercial or industrial grade solutions
produced have hypochlorite strengths of 10 to 16 percent. The stability
of sodium hypochlorite solution depends on the hypochlorite
concentration, the storage temperature, the length of storage (time),
the impurities of the solution, and exposure to light. Decomposition of
hypochlorite over time can affect the feed rate and dosage, as well as
produce undesirable byproducts such as chlorite ions or chlorate (Gordon
et al., 1995). Because of the storage problems, many systems are
investigating onsite generation of hypochlorite in lieu of its purchase
from a manufacturer or vendor (USEPA, 1998b).

#### Calcium Hypochlorite

To produce calcium hypochlorite, hypochlorous acid is made by adding
chlorine monoxide to water and then neutralizing it with a lime slurry
to create a solution of calcium hypochlorite. The water is removed from
the solution, leaving granulated calcium hypochlorite. Generally, the
final product contains up to 70 percent available chlorine and 4 to 6
percent lime. Storage of calcium hypochlorite is a major safety
consideration. It should never be stored where it is subject to heat or
allowed to contact any organic material of an easily oxidized nature
(USEPA, 1998b).

### Primary Uses and Points of Application of Chlorine

#### Uses

The main usage of chlorine in drinking water treatment is for
disinfection. However, chlorine has also found application for a variety
of other water treatment objectives such as, the control of nuisance
organisms, oxidation of taste and odor compounds, oxidation of iron and
manganese, color removal, and as a general treatment aid to filtration
and sedimentation processes (White, 1992; Connell, 1996;
Culp/Wesner/Culp, 1986). Table 2-18 presents a summary of chlorine uses
and doses.

[]{#__RefHeading___Toc450037312 .anchor}Table 2-18. Chlorine Uses and
Doses

  --------------- ----------- ---------- ------------- ----------------- ------------------
  **\             **\         **\        **\           **\               **Other
  Application**   Typical     Optimal    Reaction      Effectiveness**   Considerations**
                  Dose**      pH**       Time**                          

  Iron            0.62 mg/mg  7.0        less than 1   Good              
                  Fe                     hour                            

  Manganese       0.77 mg/mg  7--8\      1--3 hour\    Slow kinetics     Reaction time
                  Mn          9.5        minutes                         increases at lower
                                                                         pH

  Biological      1--2 mg/L   6--8       NA            Good              DBP formation
  growth                                                                 

  Taste/odor      Varies      6--8       Varies        Varies            Effectiveness
                                                                         depends on
                                                                         compound

  Color removal   Varies      4.0--6.8   Minutes       Good              DBP formation

  Zebra mussels   2--5 mg/L\             Shock level\  Good              DBP formation
                  0.2--0.5               Maintenance                     
                  mg/L^(a)^              level                           

  Asiatic clams   0.3--0.5               Continuous    Good              DBP formation
                  mg/L^(a)^                                              
  --------------- ----------- ---------- ------------- ----------------- ------------------

Notes:\
^(a)^ Residual, not dose

Sources: Adapted in part from White, 1992; Connell, 1996;
Culp/Wesner/Culp, 1986.

####  Points of Application

At conventional surface water treatment plants, chlorine is typically
added for prechlorination at either the raw water intake or flash mixer,
for intermediate chlorination ahead of the filters, for postchlorination
at the filter clearwell, or for rechlorination of the distribution
system (Connell, 1996). Table 2-19 summarizes the typical uses for each
point of application.

[]{#__RefHeading___Toc450037313 .anchor}Table 2-19. Typical Chlorine
Points of Application and Uses

  -------------------------- --------------------------------------------
  **Point of Application**   **Typical Uses**

  Raw Water Intake           Zebra mussel and Asiatic clam control,
                             control biological growth

  Flash Mixer (prior to      Disinfection, iron and manganese oxidation,
  sedimentation)             taste and odor control, oxidation of
                             hydrogen sulfide

  Filter Influent            Disinfection, control biological growth in
                             filter, iron and manganese oxidation, taste
                             and odor control, algae control, color
                             removal

  Filter Clearwell           Disinfection

  Distribution System        Maintain disinfectant residual
  -------------------------- --------------------------------------------

Sources: Connell, 1996; White, 1992; AWWA, 1990.

#### Typical Doses

Table 2-20 shows the typical dosages for the various forms of chlorine.
The wide range of chlorine gas dosages most likely represents its use as
both an oxidant and a disinfectant. While sodium hypochlorite and
calcium hypochlorite can also serve as both an oxidant and a
disinfectant, their higher cost may limit their use.

[]{#__RefHeading___Toc450037314 .anchor}Table 2-20. Typical Chlorine
Dosages at Water Treatment Plants

  --------------------------------- -------------------------------------
  **Chlorine Compound**             **Range of Doses**

  Calcium hypochlorite              0.5--5 mg/L

  Sodium hypochlorite               0.2--2 mg/L

  Chlorine gas                      1--16 mg/L
  --------------------------------- -------------------------------------

> Source: SAIC, 1998, as adapted from EPA\'s review of public water
> systems\' Initial Sampling Plans which were required by EPA's
> Information Collection Rule (ICR)

### Pathogen Inactivation and Disinfection Efficacy

#### Inactivation Mechanisms

Research has shown that chlorine is capable of producing lethal events
at or near the cell membrane as well as affecting DNA. In bacteria,
chlorine was found to adversely affect cell respiration, transport, and
possibly DNA activity (Haas and Engelbrecht, 1980). Chlorination was
found to cause an immediate decrease in oxygen utilization in both
*Escherichia coli* and *Candida parapsilosis* studies. The results also
found that chlorine damages the cell wall membrane, promotes leakage
through the cell membrane, and produces lower levels of DNA synthesis
for *Escherichia coli*, *Candida parapsilosis,* and *Mycobacterium
fortuitum* bacteria. This study also showed that chlorine inactivation
is rapid and does not require bacteria reproduction (Haas and
Engelbrecht, 1980). These observations rule out mutation or lesions as
the principal inactivation mechanisms since these mechanisms require at
least one generation of replication for inactivation to occur.

#### Environmental Effects

Several environmental factors influence the inactivation efficiency of
chlorine, including water temperature, pH, contact time, mixing,
turbidity, interfering substances, and the concentration of available
chlorine. In general, the highest levels of pathogen inactivation are
achieved with high chlorine residuals, long contact times, high water
temperature, and good mixing, combined with a low pH, low turbidity, and
the absence of interfering substances. Of the environmental factors, pH
and temperature have the most impact on pathogen inactivation by
chlorine. The effect of pH and temperature on pathogen inactivation are
discussed below.

**pH.** The germicidal efficiency of hypochlorous acid (HOCl) is much
higher than that of the hypochlorite ion (OCl^-^). The distribution of
chlorine species between HOCl and OCl^-^ is determined by pH, as
discussed above. Because HOCl dominates at low pH, chlorination provides
more effective disinfection at low pH. At high pH, OCl^-^ dominates,
which causes a decrease in disinfection efficiency.

The inactivation efficiency of gaseous chlorine and hypochlorite is the
same at the same pH after chlorine addition. Note, however, that
addition of gaseous chlorine will decrease the pH (see Equation 1) while
the addition of hypochlorite will increase the pH of the water (see
Equation 3 and Equation 4). Therefore, without pH adjustment to maintain
the same treated water pH, gaseous chlorine will have greater
disinfection efficiency than hypochlorite.

The impact of pH on chlorine disinfection has been demonstrated in the
field. For example, virus inactivation studies have shown that 50
percent more contact time is required at pH 7.0 than at pH 6.0 to
achieve comparable levels of inactivation. These studies also
demonstrated that a rise in pH from 7.0 to 8.8 or 9.0 requires six times
the contact time to achieve the same level of virus inactivation (Culp
and Culp, 1974). Although these studies found a decrease in inactivation
with increasing pH, some studies have shown the opposite effect. A 1972
study reported that viruses were more sensitive to free chlorine at high
pH than at low pH (Scarpino et al., 1972).

**Temperature.** For typical drinking water treatment temperatures,
pathogen inactivation increases with temperature. Virus studies indicate
that the contact time should be increased by two to three times to
achieve comparable inactivation levels when the water temperature is
lowered by 10°C (Clarke et al., 1962).

#### Disinfection Efficacy

Since its introduction, numerous investigations have been made to
determine the germicidal efficiency of chlorine. Although there are
widespread differences in the susceptibility of various pathogens, the
general order of increasing chlorine disinfection difficulty are
bacteria, viruses, and then protozoa.

**Bacteria Inactivation.** Chlorine is an extremely effective
disinfectant for inactivating bacteria. A study conducted during the
1940s investigated the inactivation levels as a function of time for *E.
coli*, *Pseudomonas aeruginosa*, *Salmonella typhi*, and *Shigella
dysenteriae* (Butterfield et al., 1943). Study results indicated that
HOCl is more effective than OCl^-^ for inactivation of these bacteria.
These results have been confirmed by several researchers that concluded
that HOCl is 70 to 80 times more effective than OCl^-^ for inactivating
bacteria. (Culp/Wesner/Culp, 1986).

**Virus Inactivation.** Chlorine has been shown to be a highly effective
viricide. One of the most comprehensive virus studies was conducted in
1971 using treated Potomac estuary water (Liu et al., 1971). The tests
were performed to determine the resistance of 20 different enteric
viruses to free chlorine under constant conditions of 0.5 mg/L free
chlorine and a pH and temperature of 7.8 and 2°C, respectively. In this
study, the least resistant virus was found to be reovirus and required
2.7 minutes to achieve 99.99 percent inactivation (4 log removal). The
most resistant virus was found to be a poliovirus, which required more
than 60 minutes for 99.99 inactivation. The corresponding CT range
required to achieve 99.99 percent inactivation for all 20 viruses was
between 1.4 to over 30 mg·min/L.

Virus survival studies have also been conducted on a variety of both
laboratory and field strains (AWWA, 1979). All of the virus inactivation
tests in this study were performed at a free chlorine residual of 0.4
mg/L, a pH of 7.0, a temperature of 5^o^C, and contact times of either
10, 100, or 1,000 minutes. Test results showed that of the twenty
cultures tested only two poliovirus strains reached 99.99 percent
inactivation after 10 minutes (CT = 4 mg·min/L), six poliovirus strains
reached 99.99 percent inactivation after 100 minutes (CT = 40 mg·min/L),
and 11 of the 12 polioviruses plus one *Coxsackievirus* strain (12 out
of a total of 20 viruses) reached 99.99 percent inactivation after 1,000
minutes (CT = 400 mg·min/L).

**Protozoa Inactivation.** Chlorine has been shown to have limited
success inactivating protozoa. Data obtained during a 1984 study
indicated that the resistance of *Giardia* cysts are two orders of
magnitude higher than that of enteroviruses and more than three orders
of magnitude higher than the enteric bacteria (Hoff et al., 1984). CT
requirements for *Giardia* cysts inactivation when using chlorine as a
disinfectant has been determined for various pH and temperature
conditions (AWWA, 1991). These CT values increase at low temperatures
and high pH (See also Table 2-13).

Chlorine has little impact on the viability of *Cryptosporidium* oocysts
when used at the relatively low doses encountered in water treatment
(e.g., 5 mg/L). Approximately 40 percent removals (0.2 log) of
*Cryptosporidium* were achieved at CT values of both 30 and 3,600
mg·min/L (Finch et al., 1994). Another study determined that "no
practical inactivation was observed" when oocysts were exposed to free
chlorine concentrations ranging from 5 to 80 mg/L at pH 8, a temperature
of 22°C, and contact times of 48 to 245 minutes (Gyürék et al., 1996).
CT values ranging from 3,000 to 4,000 mg·min/L were required to achieve
1-log of *Cryptosporidium* inactivation at pH 6.0 and temperature of
22^o^C. During this study, one trial in which oocysts were exposed to 80
mg/L of free chlorine for 120 minutes was found to produce greater than
3-logs of inactivation.

#### CT Curves

Chlorine is regarded as a strong disinfectant that is effective at
inactivating bacteria and viruses, and under certain circumstances,
*Giardia*. Because of chlorine's extremely high virus inactivation
efficiency, CT values are almost always governed by protozoa
inactivation. For example, Figure 2-1 shows the CT values required to
achieve between 0.5 and 3-logs of virus and *Giardia* inactivation
(AWWA, 1991). As shown, the CT values required to achieve the
recommended disinfection efficiency for conventional filtration systems
(i.e., 0.5-log *Giardia* cyst and 2-log virus inactivation level) are 23
and 3 mg min/L, respectively.

![](media/image2.wmf){width="4.54375in" height="2.8020833333333335in"}

[]{#__RefHeading___Toc450037317 .anchor}Figure 2-1. Free Chlorine
*Giardia* and Virus CT Requirements

CT values for *Giardia* inactivation for various pH values and
temperatures at a chlorine dose of 3.0 mg/L are shown in Figures 2-2 and
2-3. As shown, the inactivation efficacy of free chlorine decreases with
increasing pH and/or decreasing temperature. CT values shown in Figures
2-2 and 2-3 are based on animal infectivity and excystation studies. CT
values ranging from 0.5 to 3-log inactivation at temperatures of 0.5 and
5^o^C were based on a multiplicative model, and applying first order
kinetics to the 99 percent upper confidence interval of the
99.99-percentile CT values. CT values for temperatures above 5^o^C were
estimated by assuming a twofold decrease for every 10^o^C decrease in
temperature.

![](media/image3.wmf){width="4.7243055555555555in"
height="2.8409722222222222in"}

[]{#__RefHeading___Toc450037318 .anchor}Figure 2-2. CT Values for
Inactivation of *Giardia* Cysts by Free Chlorine at 10^o^C (at Cl~2~
dose of 3.0 mg/L)

![](media/image4.wmf){width="4.7243055555555555in"
height="2.886111111111111in"}

[]{#__RefHeading___Toc450037319 .anchor}Figure 2-3. CT Values for
Inactivation of *Giardia* Cysts by Free Chlorine at pH 7.0 (at Cl~2~
dose of 3.0 mg/L)

### DBP Formation and Control 

#### DBP Formation

Halogenated organics are formed when natural organic matter (NOM) reacts
with free chlorine or free bromine. Free chlorine is normally introduced
into water directly as a primary or secondary disinfectant. Free bromine
results from the oxidation by chlorine of the bromide ion in the source
water. Factors affecting the formation of these halogenated DBPs include
type and concentration of NOM, chlorine form and dose, time, bromide ion
concentration, pH, organic nitrogen concentration, and temperature.
Organic nitrogen significantly influenced the formation of nitrogen
containing DBPs, including haloacetonitriles, halopicrines, and cyanogen
halides (Reckhow et al., 1990; Hoigné and Bader, 1988).

The formation of DBPs is strongly related to TOC at the point of
disinfection. DBP formation also correlates with the amount of chlorine
consumed (Singer et al., 1995). Stevens et al. (1989) found that higher
TTHM formation occurs at high pH (9.4) than at low pH (5.0) while HAA
showed no clear trend as a function of pH. A survey of 35 water
utilities conducted by MWDSC (Krasner et al., 1989) showed the median
TTHM and HAA concentrations measured as 39 and 19 µg/L (i.e. more THMs
than HAAs are formed). However, a subsequent study by Singer et al.
(1995) found a reversal in dominance, with more HAAs than THMs produced
in waters from North Carolina utilities. They postulated that the reason
for this change is due to the lower pH levels and differences in TOC and
bromide concentrations in the North Carolina waters. Pourmoghaddas et
al. (1993) showed that brominated and mixed brominated/chlorinated THMs
and HAAs are formed when using chlorine in the presence of bromide.

The occurrence of THMs and HAAs is important because regulatory limits
are placed on both groups of compounds. One water utility may therefore
find that its chlorination practice is limited by the production of
THMs, while another will find that HAAs limit the use of chlorine. This
distribution of THMs and HAA is a function of the TOC and bromide
concentration in the water, as well as the pH during chlorination.

Of note, Chlorate is produced as a byproduct when hypochlorite degrades
during storage.

####  DBP Control

DBPs can be controlled by several means, including removing the DBP
precursors, modifying the chlorination strategy, changing disinfectants,
or removing the DBP itself. Because DBPs are difficult to remove once
they are formed, control strategies typically focus on the first three
methods.

Studies have shown that removal of TTHM precursors tends to remove the
formation potential for the other DBPs. Generally, aggregate DBP
formation will decrease as the removal of TOC increases. Recent research
indicates that moving the point of chlorination back into the treatment
process can reduce the formation of DBPs.

Summers et al. (1997) recently summarized the results from four studies
evaluating the impact of pretreatment on DBP formation. Jar tests were
conducted to simulate the water treatment through rapid mix,
coagulation, flocculation, and sedimentation. Chlorine was added at
various points in the jar testing to simulate the impact of various dose
points on production of DBPs. The results clearly demonstrate the
benefits of delaying the point of chlorination downstream in the
treatment train to take advantage of precursor removal during initial
flocculation and sedimentation processes. Table 

2-21 summarizes the results from this study.

[]{#__RefHeading___Toc450037315 .anchor}Table 2-21. Percent Reduction in
DBP Formation by Moving\
Chlorination Point Later In Treatment Train

+--------------+-------------+-------------+-------------+-------------+
| **           | **TTHM\     | **TTHM\     | **HAA5**    | **HAA5\     |
| Chlorination | Baseline    | Enhanced    |             | Enhanced    |
| point**      | (%)**       | (%)**       | **Baseline  | (%)**       |
|              |             |             | (%)**       |             |
+--------------+-------------+-------------+-------------+-------------+
| Pre rapid    | Basis       | 17          | Basis       | 4.7         |
| mix          |             |             |             |             |
+--------------+-------------+-------------+-------------+-------------+
| Post rapid   | 1.6         | 21          | 5.3         | 21          |
| mix          |             |             |             |             |
+--------------+-------------+-------------+-------------+-------------+
| Mid          | 8.7         | 36          | 14          | 36          |
| flocculation |             |             |             |             |
+--------------+-------------+-------------+-------------+-------------+
| Post         | 21          | 48          | 35          | 61          |
| s            |             |             |             |             |
| edimentation |             |             |             |             |
+--------------+-------------+-------------+-------------+-------------+

Notes: Source: USEPA, 1997b based on Summers et al., 1997.\
Baseline = Baseline coagulant (alum) dose for optimal turbidity removal
(\~30 mg/L)\
Enhanced = Enhanced coagulant (alum) dose for optimal TOC removal (\~52
mg/L)

Table 2-21 also shows the benefit of enhanced coagulation to reduce DBP
production. The THM reduction of 21 percent by moving the chlorination
point to post sedimentation is more than doubled to 48 percent by
enhanced coagulation. The HAA removal increases from 45 to 61 percent
under enhanced coagulation with post sedimentation chlorination.
Therefore, DBP control by selecting the optimal dose location and
conditions along with enhanced precursor removal can significantly
reduce DBP formation at low added cost.

White (1992) suggested that pretreatment goals should include: 1)
maximizing THM precursor removal; 2) reducing ammonia-N concentration to
0.10 mg/L; 3) reducing organic-N concentration to 0.05 mg/L; and 4)
limiting 15-minute chlorine demand to 0.5 mg/L. These guidelines should
improve raw water quality sufficiently to allow the use of the free
chlorine residual process without exceeding the EPA MCLs for TTHMs.

### Operational Considerations

#### Application Methods

Different application methods are used, depending upon the form of
chlorine used. The following paragraphs describe the typical application
methods for chlorine, sodium hypochlorite, and calcium hypochlorite.

**Chlorine.** Liquefied chlorine gas is typically evaporated to gaseous
chlorine prior to metering. The heat required for evaporation can be
provided through either a liquid chlorine evaporator or the ambient heat
input to the storage container. Once the compressed liquid chlorine is
evaporated, chlorine gas is typically fed under vacuum conditions.
Either an injector or a vacuum induction mixer usually creates the
required vacuum. The injector uses water flowing through a venturi to
draw the chlorine gas into a side stream of carrier water to form a
concentrated chlorine solution. This solution is then introduced into
the process water through a diffuser or mixed with a mechanical mixer. A
vacuum induction mixer uses the motive forces of the mixer to create a
vacuum and draws the chlorine gas directly into the process water at the
mixer.

**Sodium Hypochlorite.** Sodium hypochlorite solutions degrade over
time. For example, a 12.5 percent hypochlorite solution will degrade to
10 percent in 30 days under "best case" conditions (White, 1992).
Increased temperature, exposure to light, and contact with metals
increase the rate of sodium hypochlorite degradation (Connell, 1996).

Sodium hypochlorite solution is typically fed directly into the process
water using a type of metering pump. Similar to chlorine solution,
sodium hypochlorite is mixed with the process water with either a
mechanical mixer or induction mixer. Sodium hypochlorite solution is
typically not diluted prior to mixing to reduce scaling problems.

**Calcium Hypochlorite.** Commercial high-level calcium hypochlorite
contains at least 70% available chlorine (USEPA, 1991). Under normal
storage conditions, calcium hypochlorite loses 3 to 5% of its available
chlorine in a year (AWWA and ASCE, 1997). Calcium hypochlorite comes in
powder, granular, and compressed tablet forms (USEPA, 1991). Typically,
calcium hypochlorite solution is prepared by mixing powdered or granular
calcium hypochlorite with a small flow. The highly chlorinated solution
is then flow paced into drinking water flow.

#### Safety and Handling Considerations

**Chlorine.** Chlorine gas is a strong oxidizer. The U.S. Department of
Transportation classifies chlorine as a poisonous gas (Connell, 1996).
Fire codes typically regulate the storage and use of chlorine. In
addition, facilities storing more than 2,500 pounds of chlorine are
subject to the following two safety programs:

-   Process Safety Management standards regulated by the Occupational
    Safety and Health Administration under 29 CFR 1910.

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-   The Risk Management Program Rule administered by EPA under Section
    112(r) of the Clean Air Act.

All of these regulations (as well as local and state codes and
regulations) must be considered during the design and operation of
chlorination facilities at a water treatment plant.

**Sodium Hypochlorite.** Sodium hypochlorite solution is a corrosive
liquid with an approximate pH of 12 (AWWA, 1990). Therefore, typical
precautions for handling corrosive materials such as avoiding contact
with metals, including stainless steel, should be used.

Sodium hypochlorite solutions may contain chlorate. Chlorate is formed
during the both the manufacturing and storage of sodium hypochlorite
(due to degradation of the product). Chlorate formation can be minimized
by reducing the degradation of sodium hypochlorite (Gilbert et al.,
1995) by limiting storage time, avoid high temperatures and reduce light
exposure.

Spill containment must be provided for the sodium hypochlorite storage
tanks. Typical spill containment structures include containment for the
entire contents of the largest tank (plus freeboard for rainfall or fire
sprinklers), no uncontrolled floor drains, and separate containment
areas for each incompatible chemical.

**Calcium Hypochlorite.** Calcium hypochlorite is an oxidant and as such
should be stored separately from organic materials that can be readily
oxidized. It should also be stored away from sources of heat. Improperly
stored calcium hypochlorite has caused spontaneous combustion fires
(White, 1992).

## Summary

### Advantages and Disadvantages of Chlorine Use

The following list presents selected advantages and disadvantages of
using chlorine as a disinfection method for drinking water (Masschelein,
1992; Process Applications, Inc., 1992). Because of the wide variation
of system size, water quality, and dosages applied, some of these
advantages and disadvantages may not apply to a particular system.

**Advantages**

-   Oxidizes soluble iron, manganese, and sulfides

-   Enhances color removal

-   Enhances taste and odor

-   May enhance coagulation and filtration of particulate contaminants

-   Is an effective biocide

-   Is the easiest and least expensive disinfection method, regardless
    of system size

-   Is the most widely used disinfection method, and therefore, the best
    known

-   Is available as calcium and sodium hypochlorite. Use of these
    solutions is more advantageous for smaller systems than chlorine gas
    because they are easier to use, are safer, and need less equipment
    compared to chlorine gas

-   Provides a residual.

**Disadvantages**

-   May cause a deterioration in coagulation/filtration of dissolved
    organic substances

-   Forms halogen-substituted byproducts

-   Finished water could have taste and odor problems, depending on the
    water quality and dosage

-   Chlorine gas is a hazardous corrosive gas

-   Special leak containment and scrubber facilities could be required
    for chlorine gas

-   Typically, sodium and calcium hypochlorite are more expensive than
    chlorine gas

-   Sodium hypochlorite degrades over time and with exposure to light

-   Sodium hypochlorite is a corrosive chemical

-   Calcium hypochlorite must be stored in a cool, dry place because of
    its reaction with moisture and heat

-   A precipitate may form in a calcium hypochlorite solution because of
    impurities, therefore, an antiscalant chemical may be needed

-   Higher concentrations of hypochlorite solutions are unstable and
    will produce chlorate as a byproduct

-   Is less effective at high pH

-   Forms oxygenated byproducts that are biodegradable and which can
    enhance subsequent biological growth if a chlorine residual is not
    maintained.

-   Release of constituents bound in the distribution system (e.g.,
    arsenic) by changing the redox state.

### Summary Table

Table 2-22 presents a summary of the considerations for the use of
chlorine as a disinfectant.

[]{#__RefHeading___Toc450037316 .anchor}Table 2-22. Summary of Chlorine
Disinfection

  ------------------- ----------------------------------------------------
  **Consideration**   **Description**

  Generation          Chlorination may be performed using chlorine gas or
                      other chlorinated compounds that may be in liquid or
                      solid form. Chlorine gas can be generated by a
                      number of processes including the electrolysis of
                      alkaline brine or hydrochloric acid, the reaction
                      between sodium chloride and nitric acid, or the
                      oxidation of hydrochloric acid. Since chlorine is a
                      stable compound, chlorine gas, sodium hypochlorite,
                      and calcium hypochlorite are typically produced
                      off-site by a chemical manufacturer.

  Primary uses        The primary use of chlorination is disinfection.
                      Chlorine also serves as an oxidizing agent for taste
                      and odor control, prevention of algal growths,
                      maintaining clear filter media, removal of iron and
                      manganese, destruction of hydrogen sulfide, color
                      removal, maintaining the water quality at the
                      distribution systems, and improving coagulation.

  Inactivation        The general order of increasing chlorine
  efficiency          disinfection difficulty is bacteria, viruses, and
                      then protozoa. Chlorine is an extremely effective
                      disinfectant for inactivating bacteria and highly
                      effective viricide. However, chlorine is less
                      effective against *Giardia* cysts. *Cryptosporidium*
                      oocysts are highly resistant to chlorine.

  Byproduct formation When added to the water, free chlorine reacts with
                      NOM and bromide to form DBPs, primarily THMs, some
                      haloacetic acids (HAAs), and others.

  Point of            Raw water storage, precoagulation/post-raw water
  application         storage, presedimentation/ postcoagulation,
                      postsedimentation/prefiltration, post filtration
                      (disinfection), or in the distribution system.

  Special             Because chlorine is such a strong oxidant and
  considerations      extremely corrosive, special storage and handling
                      considerations should be considered in the planning
                      of a water treatment plant. Additionally, health
                      concerns associated with handling and use of
                      chlorine is an important consideration.
  ------------------- ----------------------------------------------------

### Reference for Additional Information on Chlorine

With the focus of this manual on disinfectants other than chlorine, all
of chlorine's uses and capabilities are not described here. For more
detailed information regarding the use of chlorine in water treatment,
refer to the list of references provided below. For complete references,
see the References section at the end of this chapter.

-   AWWA (1990)

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-   Connell (1996)

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-   DeMers and Renner (1992)

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-   Hazen and Sawyer (1992)

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-   Hoigné and Bader (1988)

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-   Sawyer et al. (1994)

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-   Singer (1988)

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-   White (1992)

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     *J. Hygiene*. 8:538.

101. White, G.C. 1992. *Handbook of Chlorination and Alternative
     Disinfectants*. Van Nostrand Reinhold, New York, NY.

102. Witherell, L.E, R.W. Duncan, K.M. Stone, L.J. Stratton, L.
     Orciari, S. Kappel, D.A. Jillson. 1988. "Investigation of
     Legionella Pneumophila in Drinking Water." *J. AWWA*. 80 (2):88-93.

Disinfectant Use in Water Treatment
[2-1](#disinfectant-use-in-water-treatment)

2.1 Need for Disinfection in Water Treatment
[2-1](#need-for-disinfection-in-water-treatment)

2.1.1 Pathogens of Primary Concern [2-2](#pathogens-of-primary-concern)

2.1.2 Recent Waterborne Outbreaks [2-8](#recent-waterborne-outbreaks)

2.1.3 Mechanism of Pathogen Inactivation
[2-9](#mechanism-of-pathogen-inactivation)

2.2 Other Uses of Disinfectants in Water Treatment
[2-10](#other-uses-of-disinfectants-in-water-treatment)

2.2.1 Minimization of DBP Formation
[2-10](#minimization-of-dbp-formation)

2.2.2 Control of Nuisance Asiatic Clams and Zebra Mussels
[2-11](#control-of-nuisance-asiatic-clams-and-zebra-mussels)

2.2.3 Oxidation of Iron and Manganese
[2-13](#oxidation-of-iron-and-manganese)

2.2.4 Prevention of Regrowth in the Distribution System and Maintenance
of Biological Stability
[2-14](#prevention-of-regrowth-in-the-distribution-system-and-maintenance-of-biological-stability)

2.2.5 Removal of Taste and Odors Through Chemical Oxidation
[2-15](#removal-of-taste-and-odors-through-chemical-oxidation)

2.2.6 Improvement of Coagulation and Filtration Efficiency
[2-15](#improvement-of-coagulation-and-filtration-efficiency)

2.2.7 Prevention of Algal Growth in Sedimentation Basins and Filters
[2-16](#prevention-of-algal-growth-in-sedimentation-basins-and-filters)

2.2.8 Removal of Color [2-16](#removal-of-color)

2.3 Disinfection Byproducts and Disinfection Residuals
[2-16](#disinfection-byproducts-and-disinfection-residuals)

2.3.1 Types of DBPs and Disinfection Residuals
[2-16](#types-of-dbps-and-disinfection-residuals)

2.3.2 Disinfection Byproduct Formation
[2-19](#disinfection-byproduct-formation)

2.3.3 DBP Control Strategies [2-23](#dbp-control-strategies)

2.3.4 CT Factor [2-25](#ct-factor)

2.4 Pathogen Inactivation Versus DBP Formation
[2-26](#pathogen-inactivation-versus-dbp-formation)

2.5 Disinfectant Residual Regulatory Requirements
[2-27](#disinfectant-residual-regulatory-requirements)

2.6 Summary of Current National Disinfection Practices
[2-28](#summary-of-current-national-disinfection-practices)

2.7 Chlorine [2-30](#chlorine)

2.7.1 Chlorine Chemistry [2-31](#chlorine-chemistry)

2.7.2 Chlorine Generation [2-32](#chlorine-generation)

2.7.3 Primary Uses and Points of Application of Chlorine
[2-33](#primary-uses-and-points-of-application-of-chlorine)

2.7.4 Pathogen Inactivation and Disinfection Efficacy
[2-35](#pathogen-inactivation-and-disinfection-efficacy)

2.7.5 DBP Formation and Control [2-39](#dbp-formation-and-control)

2.7.6 Operational Considerations [2-41](#operational-considerations)

2.8 Summary [2-42](#summary)

2.8.1 Advantages and Disadvantages of Chlorine Use
[2-42](#advantages-and-disadvantages-of-chlorine-use)

2.8.2 Summary Table [2-44](#summary-table)

2.8.3 Reference for Additional Information on Chlorine
[2-44](#reference-for-additional-information-on-chlorine)

2.9 References [2-45](#references)

Table 2-1. Waterborne Diseases from Bacteria
[2-3](#__RefHeading___Toc450037295)

Table 2-2. Waterborne Diseases from Human Enteric Viruses
[2-4](#__RefHeading___Toc450037296)

Table 2-3*.* Waterborne Diseases from Parasites
[2-6](#__RefHeading___Toc450037297)

Table 2-4. Attributes of the Three Waterborne Pathogens of Concern in
Water Treatment [2-7](#__RefHeading___Toc450037298)

Table 2-5. Human Parasitic Protozoans
[2-7](#__RefHeading___Toc450037299)

Table 2-6. The Effects of Various Oxidants on Mortality of the Asiatic
Clam (*Corbicula fluminea*) [2-12](#__RefHeading___Toc450037300)

Table 2-7. Oxidant Doses Required for Oxidation of Iron and Manganese
[2-14](#__RefHeading___Toc450037301)

Table 2-8. List of Disinfection Byproducts and Disinfection Residuals
[2-17](#__RefHeading___Toc450037302)

Table 2-9. Status of Health Information for Disinfectants and DBPs
[2-18](#__RefHeading___Toc450037303)

Table 2-10. Conditions of Formation of DBPs
[2-22](#__RefHeading___Toc450037304)

Table 2-11. Inorganic DBPs Produced During Disinfection
[2-23](#__RefHeading___Toc450037305)

Table 2-12. Required Removal of TOC by Enhanced Coagulation for Surface
Water Systems^+^ Using Conventional Treatment^++^ (percent reduction)
[2-25](#__RefHeading___Toc450037306)

Table 2-13. CT Values for Inactivation of Viruses
[2-26](#__RefHeading___Toc450037307)

Table 2-14. CT Values for Inactivation of *Giardia* Cysts
[2-26](#__RefHeading___Toc450037308)

Table 2-15. Summary of Disinfection Impacts
[2-27](#__RefHeading___Toc450037309)

Table 2-16. Disinfection Practices of Water Systems that Include Some
Form of Treatment [2-29](#__RefHeading___Toc450037310)

Table 2-17. Ozone Application in Water Treatment Plants in the United
States [2-30](#__RefHeading___Toc450037311)

Table 2-18. Chlorine Uses and Doses [2-34](#__RefHeading___Toc450037312)

Table 2-19. Typical Chlorine Points of Application and Uses
[2-34](#__RefHeading___Toc450037313)

Table 2-20. Typical Chlorine Dosages at Water Treatment Plants
[2-35](#__RefHeading___Toc450037314)

Table 2-21. Percent Reduction in DBP Formation by Moving Chlorination
Point Later In Treatment Train [2-40](#__RefHeading___Toc450037315)

Table 2-22. Summary of Chlorine Disinfection
[2-44](#__RefHeading___Toc450037316)

Figure 2-1. Free Chlorine *Giardia* and Virus CT Requirements
[2-38](#__RefHeading___Toc450037317)

Figure 2-2. CT Values for Inactivation of *Giardia* Cysts by Free
Chlorine at 10^o^C (at Cl~2~ dose of 3.0 mg/L)
[2-38](#__RefHeading___Toc450037318)

Figure 2-3. CT Values for Inactivation of *Giardia* Cysts by Free
Chlorine at pH 7.0 (at Cl~2~ dose of 3.0 mg/L)
[2-39](#__RefHeading___Toc450037319)