EPA 749-F-94-010a

                      CHEMICAL SUMMARY FOR CHLORINE
                               prepared by
                OFFICE OF POLLUTION PREVENTION AND TOXICS
                  U.S. ENVIRONMENTAL PROTECTION AGENCY
                               August 1994

     This summary is based on information retrieved from a systematic
search limited to secondary sources (see Appendix A).  These sources
include online databases, unpublished EPA information, government
publications, review documents, and standard reference materials.  No
attempt has been made to verify information in these databases and
secondary sources.

I. CHEMICAL IDENTITY AND PHYSICAL/CHEMICAL PROPERTIES

     The chemical identity and physical/chemical properties of chlorine
are summarized in Table 1.  

TABLE 1.  CHEMICAL IDENTITY AND CHEMICAL/PHYSICAL PROPERTIES OF CHLORINE
__________________________________________________________________________

Characteristic/Property             Data             Reference
__________________________________________________________________________

CAS No.                       7782-50-5             
Common Synonyms               none                  
Molecular Formula             Cl2                   
Chemical Structure            Cl-Cl                 
Physical State                greenish yellow 
                              diatomic gas             Budavari et al. 1989
Molecular Weight              35.453                   Budavari et al. 1989
Melting Point                 -101.00C                Budavari et al. 1989
Boiling Point                 -34.05C at 760 mm Hg    Budavari et al. 1989
Water Solubility 
  (see note)                  7.3 g/L @ 20C
                              14.6 g/L @ g/L           U.S. EPA 1989
Density                       1.468 mg/L @ 0C/
                              3.65 atm                 U.S. EPA 1989
Vapor Density                 3.209-3.214 mg/L 
                                (dry gas) 
                                 @ 0C/1 atm           U.S. EPA 1989
KOC                           no data were found    
Log KOW                       no data were found    
Vapor Pressure                5.85 x 103 mm Hg @ 25C  CHEMFATE 1994
Reactivity                    highly reactive; forms 
                              explosive mixtures 
                              with flammable gases 
                              and vapors               HSDB 1994
Flash Point                   nonflammable             HSDB 1994
Henry's Law Constant          no data were found       
Fish Bioconcentration 
  Factor                      no data were found     
Odor Threshold                0.0020 mg/L (water), 
                              0.31 ppm (air)           HSDB 1994
Conversion Factors            1 ppm = 2.9 mg/m3
                              1 mg/m3= 0.34 ppm        U.S. EPA 1989

Note:  When chlorine is added to fresh water, the solution will usually 
contain two forms of free chlorine: hypochlorous acid (HOCl) and the 
hypochlorite ion (OCl ) (U.S. EPA 1985).  Other chlorinated compounds 
may be present, depending on other materials present in the water.  The 
term "total residual chlorine" is used to refer to the sum of free 
chlorine and combined chlorine in fresh water.
__________________________________________________________________________

II. PRODUCTION, USE, AND TRENDS

    A. Production
     
       There are 18 producers producing chlorine at 40 facilities in 
       the United States.  Table 2 lists producers, plant locations, 
       and plant capacities.  Annual US capacity is over 13 million 
       short tons.  In 1992, approximately 11.7 million short tons of 
       chlorine were produced in the US.  In that same year, 274,000 
       short tons of chlorine were imported into the US and 34,000 short 
       tons were exported (Mannsville 1993).

     B. Use

        Chlorine is used in a number of industrial applications.  Its 
        largest use is as a raw material in the production of ethylene 
        dichloride, an intermediate for vinyl chloride monomer and 
        polyvinyl chloride (PVC) resins.  Chlorine is also used in the 
        paper industry to bleach pulp, in the production of chlorinated 
        solvents and chlorofluorocarbons (CFCs), as a disinfectant or 
        fungicide for a variety of purposes, including water purification, 
        cooling systems, meat, fish, vegetable, and fruit processing, foot 
        baths, dairy equipment, laundries, and dishwater, as well as for
        shrink-proofing wool, in special batteries (with lithium or zinc), 
        and in the manufacture of propylene oxide and pesticides.  Table 3 
        shows the estimated 1993 end-use pattern for chlorine.

     C.   Trends

          Chlorine use in pulp bleaching and in the production of some 
          chlorinated solvents and CFCs is expected to decline due to 
          environmental concerns.  Overall, demand for chlorine is expected 
          to increase approximately 1 percent per year for a few years,
          followed by a period of moderate decline (Mannsville 1993).

            
               TABLE 2.  United States Producers of Chlorine
__________________________________________________________________________

Company                  Plant Location(s)            Plant Capacity
                                                  (in 1,000s of short tons)
__________________________________________________________________________

BF Goodrich                Calvert City, KY                  115
Dow Chemical               Freeport, TX                    2,400
                           Plaquemine, LA                  1,150
DuPont                     Niagara Falls, NY                  85
Elf Atochem                Portland, OR                      150
                           Tacoma, WA                         90
Formosa Plastics           Baton Rouge, LA                   200
                           Point Comfort, TX                 625
General Electric           Burkeville, AL                     25
                           Mt. Vernon, IN                     55
Georgia Gulf               Plaquemine, LA                    450
Georgia Pacific            Bellingham, WA                     90
                           Brunswick, GA                      30
Hanlin                     Acme, NC                           53
                           Brunswick, GA                     101
                           Orrington, ME                      80
La Roche Chemicals         Gramercy, LA                      205
Miles                      Baytown, TX                       130
Niachlor                   Niagara Falls, NY                 240
Occidental Chemical        Convent, LA                       308
                           Corpus Christi, TX                455
                           Deer Park, TX                     396
                           Delaware City, DE                 139
                           LaPorte, TX                       525
                           Mobile, AL                         42
                           Muscle Shoals, AL                 145
                           Niagara Falls, NY                 330
                           Tacoma, WA                        220
                           Taft, LA                          645
Olin                       Augusta, GA                       110
                           Charleston, TN                    255
                           McIntosh, AL                      400
Pioneer Chlor-Alkali Co.   Henderson, NV                     115
                           St. Gabriel, LA                   180
PPG Industries             Lake Charles, LA                1,265
                           Natrium, WV                       380
Vulcan Chemicals           Geismar, LA                       249
                           Wichita, KS                       255
                           Port Edwards, WI                   73
Weyerhauser                Longview, WA                      140
__________________________________________________________________________

Source:  Mannsville 1993.

    TABLE 3.  Estimated 1993 United States End-Use Pattern of Chlorine

__________________________________________________________________________  
  
Use of Chlorine                         Percentage of all Chlorine Use 
(typical Standard Industrial 
Classification (SIC) Code) (see end note 1)
__________________________________________________________________________
                                                                          
Ethylene dichloride (intermediate for PVC production) 
   (production, SIC 2869; use, 2821)                      35%
Pulp and paper (production, SIC 2621)                     11%
Propylene oxide (production, SIC 2869; 
   use, various industries)                                8%
Chlorinated ethanes (production, SIC 2869; 
    use, various industries)                               5%
Chlorinated methanes (production, SIC 2869; 
    use, various industries)                               4%
Other organic chemicals (production, SIC 286; 
     use, various industries)                             16%
Inorganic chemicals (production, SIC 281; 
     use, various industries)                             11%
Water treatment (used in various industries)               5%
Miscellaneous (no applicable SIC Code(s))                  5%
__________________________________________________________________________

Source:  Mannsville 1993.

III. ENVIRONMENTAL FATE

     A. Environmental Release

        In addition to the chlorinated water that is released into the 
        environment from sewage treatment operations and other sources, 
        chlorine is potentially released during its transport; from its 
        manufacturing/processing facilities, such as the pulp and paper
        industries and plastic and resin industries; and through the 
        disposal of consumer products containing chlorine, such as auto-
        motive fluids, household bleaches, and refrigerants (HSDB 1994; 
        NTP 1992).  Limited monitoring studies have detected chlorine in 
        the ambient atmosphere at concentrations ranging from 1 to 
        3.7 mg/m3 (0.344 to 1.27 ppm) (HSDB 1994). 
        
        In 1992, releases of chlorine to environmental media, as reported 
        to the Toxic Chemical Release Inventory by certain types of U.S. 
        industries, totaled about 69.9 million pounds to the atmosphere, 
        1.2 million pounds to surface water, 48 thousand pounds to 
        underground injection sites, and 46 thousand pounds to land 
        (TRI92 1994).

     B. Transport

        Vaporization of molecular chlorine (Cl2) from water to the 
        atmosphere may be significant at low pH values and high concentra-
        tions (e.g., pH 2 and 3500 mg/L chlorine), but is insignificant at 
        neutral pH and low concentrations (U.S. EPA 1989).

     C. Transformation/Persistence

        1. Air - Information regarding the environmental fate of chlorine 
           in air was not found in the secondary sources searched.

        2. Soil - Chlorine may react with soil components to form 
           chlorides; depending on their water solubility, these chlorides 
           are easily washed out from the soil (Seiler et al. 1988).

        3. Water - Chlorine hydrolyzes very rapidly in water (rate 
           constants range from  1.5 x 10-4 at 0C to 4.0 x 10-4 at 25C; 
           half-life in natural waters, 0.005 s) (U.S. EPA 1989).  In 
           fresh and wastewaters at pH >6, complete hydrolysis occurs with 
           the formation of hypochlorous acid (HOCl) and chloride ion 
           (Cl-).  The hypochlorous acid ionizes to hydrogen ion (H+) and 
           hypochlorite ion (OCl-).  At pH values >5, OCl- predominates; at 
           pH values <5, HOCl predominates (U.S. EPA 1989).  Free chlorine 
           (Cl2, HOCl, and OCl-) reacts rapidly with inorganics such as 
           bromide and more slowly with organic material present in natural 
           waters.  These reactions yield chloride, oxidized organics, 
           chloroganics (including trihalomethanes), oxygen, nitrogen,
           chlorate, bromate and bromoorganics.

        4. Biota - There is no potential for the bioaccumulation or 
           bioconcentration of chlorine (HSDB 1994).

     D. Chlorine in Drinking Water

        Chlorine, added to drinking water as chlorine gas (Cl2) or hypo-
        chlorite salts (e.g., NaOCl), effectively inactivates bacteria 
        in 20 minutes at concentrations of 0.03 to 0.06 mg/L at pH range 
        of 7.0 to 8.5 and temperature range of 4C to 22C (NTP 1992). 
        Data for over 80 water supplies throughout the United States 
        indicate that the facilities applied chlorine at ranges of 1 to 
        29.7 mg/L and residual levels ranged from 0.2 to 6 mg/L (HSDB 
        1994).

V.  HEALTH EFFECTS

    A. Pharmacokinetics

       1. Absorption - Following oral administration of (HO)36Cl to rats, 
          36Cl was rapidly absorbed into the blood where concentrations 
          peaked in 2 hours for fasted animals and in 4 hours for nonfasted 
          animals (U.S. EPA 1989).  

       2. Distribution - Seventy-two hours after oral administration of 
          3.26 mg/kg (HO)36Cl to male Sprague-Dawley rats, the
concentration 
          of (HO)36Cl was highest in the plasma (0.77% of initial dose), 
          followed by bone marrow, kidney, testes, lung, skin, duodenum, 
          spleen, liver and carcass, and was lowest in the ileum (U.S. 
          EPA 1989).  A similar pattern of distribution was observed 96 
          hours after administration of 2.61 mg/kg (U.S. EPA 1989).

       3. Metabolism - Free chlorine (Cl2, OCl-, or HOCl) is a strong 
          oxidizing agent that reacts readily with biological materials 
          (including proteins and nucleotide bases) to produce a variety 
          of organic chlorinated compounds (U.S. EPA 1989).  At least one 
          investigator demonstrated trihalomethanes in the plasma of rats 
          given oral doses of sodium hypochlorite (NTP 1992).  Experiments 
          in fasted rats have shown that 81% of the total 36Cl in the 
          plasma, 96 hours after administration, was in the form of 
          chloride ion (U.S. EPA 1989).

       4. Excretion - Chlorine is excreted from the body primarily in the 
          urine and feces.  Rats given oral doses of 2.61 mg/kg of (HO)36Cl 
          excreted 36.4% of the administered dose in the urine and 14.80% 
          in the feces within 96 hours of dosing (U.S. EPA 1989).  36Cl  
          compounds were not detected in expired air.

     B. Acute Effects

        1. Humans - Oral doses of 2.5 mg chlorine/day, administered to 10 
           men for 12 weeks, had no adverse effects (U.S. EPA 1990).  
           No adverse effects were noted in persons ingesting water 
           containing 50-90 ppm of chlorine (~1.4 to 2.6 mg Cl/kg/day) for 
           a short periods of time (U.S. EPA 1989).  Drinking water
           concentrations of >90 ppm chlorine caused irritation of 
           membranes of throat and mouth (U.S. EPA 1989).  Concentrations 
           of chlorine in the drinking water of greater than 25 ppm make 
           the drinking water unpalatable (U.S. EPA 1989).

           Chlorine is a primary irritant to the mucous membranes of the 
           eyes, nose, and throat and to the linings of the entire respira-
           tory tract (Stokinger 1982). The extent of acute injury to 
           humans depends on the concentration and  duration of exposure 
           as well as the water content of the tissue involved and
           the presence of underlying cardiopulmonary disease (HSDB 1994).  
           The estimated clinical effects of varying concentrations of 
           chlorine are as follows:  mild mucous membrane irritation at 
           1-3 ppm; moderate irritation of the upper respiratory tract at 
           5-15 ppm; immediate chest pain, vomiting, dyspnea, and cough 
           at 30 ppm; toxic pneumonitis and pulmonary edema at 40-60 ppm;
           death at 430 ppm for 30 minutes or 1000 ppm for a few minutes 
           (HSDB 1994).  Seventy-six individuals, exposed during a football 
           game when approximately 1100 pounds of chlorine gas were 
           released from a plant, suffered no serious or prolonged 
           incapacitation due to the release (HSDB 1994).  If one survives 
           acute exposure to chlorine, recovery is usually complete and 
           rapid (U.S.EPA 1989).

        2. Animals - LC50 values for rats and mice are  293 ppm for 1 h 
           and 137 ppm for 1 h, respectively (HSDB 1994).  LCLo values 
           for other species range from 330 ppm for 7 h (guinea pigs) to 
           660 ppm for 4 h (cats and rabbits) (U.S. EPA 1989).  Mice and 
           rats exposed to chlorine at the RD50 concentration (9-11
           ppm, 6 h/day for 1, 3, or 5 days) developed degeneration of 
           olfactory sensory cells in the olfactory mucosa, loss of cilia 
           of the respiratory epithelium, and cellular exfoliation, 
           primarily of the naso- and maxilloturbinates (HSDB 1994).
           Signs and symptoms of the acute oral toxicity of chlorine in 
           rats include decreased blood glutathione (30 minutes after 0.2 
           mg chlorine/kg administered as HOCl); decreased hypothalamic 
           norepinephrine levels and increases in normetanephrine levels 
           (3 and 24 hours after intubation of 250 mg/kg free chlorine as 
           HOCl); morphological and biochemical liver changes (within 
           2 days of dosing with 142.9 mg/kg free chlorine as NaOCl); 
           kidney enlargement (200 mg/kg/day available chlorine for 14 
           days) (U.S. EPA 1989); and dose-related increase in liver and 
           kidney weights (210 mg dietary chlorine/kg body weight/day for 
           28 days) (U.S. EPA 1987).  C57Bl/6N mice given chlorine (25-30 
           ppm) in the drinking water for one to three weeks had signi-
           ficant decreases in the number of peritoneal exudate
macrophages, 
           and decreased in vitro cytotoxicity against mouse melanoma (B16) 
           and fibrosarcoma (UV-112) target cells (U.S. EPA 1989).

     C. Subchronic/Chronic Effects

        The major target organs for the subchronic/chronic toxicity of 
        chlorine in humans are the respiratory tract and the blood.  The 
        major target organs for the subchronic/chronic toxicity of chlorine 
        in animals are the immune system, the blood, the cardiovascular 
        system and the respiratory tract.  EPA has derived an oral RfD
        (reference dose) (see end note 3) of 0.1 mg/kg/day for chlorine, 
        based on a no-observed-adverse-effect level of 14.4 mg/kg/day in 
        a chronic drinking water study in rats.

        1. Humans - Fifty-five workers exposed to about 1.0 ppm of 
           chlorine, 8 h/day for at least 90 days exhibited (based on 
           reported symptoms and x-rays) asthma, chronic bronchitis, 
           tuberculosis, and emphysema (U.S. EPA 1987).  The concentration 
           of 1 ppm is roughly equivalent to 0.415 mg/kg/day (see end note
4).  
           In one case study, exposure to 0.015 mg/L of chlorine, 8 h/day 
           for 6 years resulted in dyspnea, marked emphysema of both lower 
           lung lobes, and reduced respiratory mobility (U.S. EPA 1987).

           Fifteen male workers exhibited decreased residual levels of 
           maximal mid-expiratory flow rates and FEV/FVC after exposure to 
           0.18 ppm chlorine, 8 h/day, 5 days/week for 8.9 years 
           (U.S. EPA 1990).  Workers in 25 chlor-alkali plants (332 males), 
           exposed to chlorine concentrations of 0.006 to 1.42 ppm (8-h 
           TWAs) for about 10.9 years showed no dose-related correlation 
           between chlorine exposure and the prevalence of colds, dyspnea, 
           palpitation, chest pain, or permanent lung damage (544 exposed 
           workers had chest x-rays) (Stokinger 1982).  Electrocardiograms 
           were abnormal in 9.4% of the exposed workers, compared with 
           8.5% of unexposed controls, and the incidence of fatigue was 
           increased in workers exposed to >0.5 ppm.  There were small
           correlations between exposure to chlorine and anxiety and 
           dizziness (p = 0.02), leukocytosis (p<0.05) and decreased 
           hematocrit (p< 0.017).  A smaller study included 52 workers 
           exposed to about 0.289 ppm chlorine for 10 years (Stokinger 
           1982).  These workers exhibited a slightly significant, 
           lower value for a single pulmonary function test.

        2. Animals - Groups of 70 F344/N male and female rats were given 
           drinking water containing  up to 275 ppm of chlorine (14.4 
           mg/kg/day) for 2 years.  No hematologic abnormalities were 
           detected at interim sacrifices (14 and 66 weeks) and no 
           non neoplastic abnormalities were observed in extensive gross 
           and microscopic examinations at the end of the study 
           (NTP 1992).  The EPA used the no-observed-adverse-effect 
           level, 14.4 mg/kg/day, to calculate a chronic oral RfD of 
           0.1 mg/kg/day for chlorine (U.S. EPA 1994).

           Sprague-Dawley rats, given 5, 15, or 30 ppm chlorine in 
           drinking water from weaning to 12 weeks of age exhibited 
           significantly reduced spleen weights, suppressed delayed-type 
           hypersensitivity reactions, and decreased oxidative metabolism 
           by macrophages at the highest dose; no effects were noted for
           the other doses or on other parameters of immunotoxicity 
           (NTP 1992).  F344 rats given doses of chlorine up to 60 mg/kg/
           day for 92 days exhibited no histopathology in major organs 
           (U.S. EPA 1989).  Other species, exposed subchronically to 
           chlorine exhibited the following:  mice had no adverse effects 
           on weight gain, food or water consumption, histological 
           parameters (12.5 mg/kg/day for 50 days or 25 mg/kg/day for 
           33 days) (U.S. EPA 1989); New Zealand rabbits had increased 
           hydroxyproline levels in heart tissue (1.6 mg chlorine/kg/day 
           for 3 months; no effect at 0.1 mg/kg/day) (U.S. EPA 1989); 
           Carneau pigeons exhibited cardiovascular effects (10 mg
chlorine/
           kg/day in drinking water for 9 months) (U.S. EPA 1989).

           In various studies, Sprague Dawley and F344 rats treated with 
           chlorine orally for 12-24 months at doses ranging from 0.14 to 
           22 mg/kg/day exhibited one or more of the following symptoms:  
           significant decreases in red blood cell count and hematocrit 
           (reversed at 6 months), increased osmotic fragility, increased 
           mean corpuscular hemoglobin, significant decreases in body and
           liver weights, decreased brain and heart weights (p<0.05), and 
           decreased salivary gland and kidney weights (U.S. EPA 1989), 
           decreased spleen weight, and decreased thyroid weight (U.S. 
           EPA 1987).

           Rhesus monkeys (4/sex/dose) exposed to 2.3 ppm of chlorine 
           6 h/day, 5 days/week for 1 year experienced ocular irritation, 
           conjunctival irritation, hyperplasia of the nasal mucosa, and, 
           in some females, epithelial hyperplasia of the trachea with 
           minimal evidence of early nonkeratinizing squamous metaplasia 
           (U.S. EPA 1990).

     D. Carcinogenicity

        No conclusion on the carcinogenicity of chlorine can be made based 
        on the limited information available from human and animal studies. 

        1. Humans - NTP (1992) notes that some epidemiologic studies have 
           shown an association between the consumption of chlorinated 
           drinking water and an increased risk for the development of 
           cancer, primarily of the urinary tract.  EPA has established 
           drinking water standards for several chlorinated by-products 
           found in chlorinated drinking water.

        2. Animals - F344/N male and female rats and B6C3F1 male and female 
           mice (50/sex/group) received 0, 70, 140, or 275 ppm chlorine 
           (based on atomic chlorine) in their drinking water for 2 years. 
           (NTP 1992).  The female rats had a slignt increase in the 
           incidence of mononuclear cell leukemia that was not clearly 
           dose-related (control, 8/50; low-dose, 7/50; mid-dose, 19/51; 
           high-dose, 16/50), but was considered by the NTP to be 
           "equivocal evidence of carcinogenic activity".  There was 
           "no evidence of carcinogenic activity" in male rats or male and 
           female mice at the doses tested.

           In another study, chlorine administered as NaOCl to rats in 
           drinking water at levels up to 1000 mg/L for males and 200 mg/L 
           for females was not carcinogenic (NTP 1992).  Information on the 
           cocarcinogenicity of sodium hypochlorite are conflicting.  When 
           applied to the skin of mice, sodium hypochlorite enhanced tumor 
           development initiated by 4-nitroquinoline-1-oxide and reduced 
           tumor development initiated by benzo[a]pyrene (U.S. EPA 1989).

     E. Genotoxicity

        Chlorine was mutagenic in Salmonella typhimurium strains TA1530 
        and TA100, without metabolic activation; produced chromosome 
        aberrations in human lymphocytes and other mammalian cells 
        (20 ppm); interacted with DNA in E. coli polA test (as sodium 
        hypochlorite); and was negative for the induction of erythrocyte
        micronuclei or chromosome aberrations of bone marrow cells of 
        Swiss CD-1 mice (up to 8 mg/kg/day of NaOCl) for up to 5 days 
        (U.S. EPA 1989).

     F. Developmental/Reproductive Toxicity

        No conclusion on the developmental/reproductive toxicity of 
        chlorine can be made based on the limited information available 
        from human and animal studies. 

        1. Humans - No information was found in the secondary sources 
           searched to indicate that chlorine is a developmental/
           reproductive toxicant in humans.

        2. Animals - Female Sprague-Dawley rats were given chlorine 
           concentrations of 0, 1.0, 10, or 100 mg/L in the drinking water 
           (as HOCL) for 2.5 months prior to conception and throughout 
           gestation, were killed on gestation day 20, and the fetuses 
           were examined (NTP 1992).  Resorptions were not increased
           at any concentration; however, fetuses in the 100 mg/L group 
           had soft tissue defects, including improper orientation of the 
           heart and adrenal agenesis, and a slightly increased incidence 
           of skeletal variants, such as incompletely ossified or missing 
           sternebrae or rudimentary ribs.  Statistical analyses were
           not available.  In other studies, chlorine administered to 
           pregnant mice was negative for reproductive and teratogenic 
           effects when given in drinking water as 10-13 ppm of sodium 
           hypochlorite and hydrochloric acid (to maintain water pH of 2.5) 
           or when given in heavily chlorinated municipal drinking water 
           (U.S. EPA 1989). 

           Sperm head abnormalities were observed in B6C3F1 mice given 
           1.6 and 4.0 mg/kg/day of chlorine as OCl-, but not at 8.0 
           mg/kg or when given as HOCl (U.S. EPA 1994).  BDII rats (236 
           total males and females) given 10 mg/kg/day of free residual 
           chlorine in the drinking water throughout 7 generations had no 
           adverse effects on weight gain, food consumption, water
           consumption, fertility, lifespan, growth pattern, hematology, 
           histology (liver, spleen, kidney or other organs) 
           (U.S. EPA 1989).

     G. Neurotoxicity

        No information was found in the secondary sources searched 
        regarding the neurotoxicity of chlorine.

V. ENVIRONMENTAL EFFECTS
     
   A. Toxicity to Aquatic Organisms

       Chlorine has high acute toxicity to aquatic organisms; many toxicity 
       values are less than or equal to 1 mg/L.  Twenty-four-hour LC50 
       values range from 0.076 to 0.16 mg/L for Daphnia magna (water flea) 
       and from 0.005 to 0.1 mg/L for Daphnia pulex (cladocern) 
       (AQUIRE 1994); 48-hour LC50 values range from 5.3 to 12.8 mg/L for
       Nitocra spinipes (snail); and 96-hour LC50 values range from 0.13 
       to 0.29 mg/L for Oncorhynchus mykiss (rainbow trout), from 0.1 to 
       0.18 mg/L for Salvelinus fontinalis (brook trout), and from 
       0.71-0.82 mg/L for Lepomis cyanellus (green sunfish) (AQUIRE 1994). 
       Papillomas of the oral cavity in fish have been associated
       with exposure to chlorinated water supplies (NTP 1992).

       Low level chlorination (0.05 to 0.15 mg/L) results in significant 
       shifts in the species composition of marine phytoplankton 
       communities (HSDB 1994).

    B. Toxicity to Terrestrial Organisms

       Chlorine is phytotoxic but is also essential to plant growth; crops 
       need around 5 pounds or more of chlorine per acre.  Acute toxicity 
       to plants is characterized by defoliation with no leaf symptoms and, 
       in higher plant forms, by spotting of the leaves (at 1.5 mg/m3) 
       and marginal and interveinal injury (at 150-300 mg/m3) (Seiler 
       et al. 1988).  No data were found in the secondary sources 
       searched regarding the toxicity of chlorine to terrestrial animals; 
       however, the data from experimental studies indicate that injury 
       to animals would occur only in the presence of high concentrations 
       of chlorine, either in drinking water or the ambient atmosphere.

    C. Abiotic Effects

       Information regarding the abiotic effects of chlorine was not found 
       in the secondary sources searched.     

VI.  EPA/OTHER FEDERAL/OTHER GROUP ACTIVITY
     
     The Clean Air Act Amendments of 1990 list chlorine as a hazardous 
     air pollutant.  Occupational exposure to chlorine is regulated by the 
     Occupational Safety and Health Administration.  The permissible 
     exposure limit (PEL) is 1 part per million parts of air (ppm) or
     3 mg/m3 as a ceiling value (i.e., exposures may not exceed these 
     levels) (29 CFR 1910.1000).

     Federal agency and other group activities for chlorine are summarized 
     in Tables 4 and 5.

  TABLE 4.  EPA OFFICES AND CONTACT NUMBERS FOR INFORMATION ON CHLORINE
_________________________________________________________________________
EPA OFFICE            LAW                                 PHONE NUMBER
_________________________________________________________________________
Pollution Prevention  Toxic Substances Control Act        (202) 554-1404
 & Toxics               (Sec. 8A/8D/8E)
                      Emergency Planning and Community
                       Right-to-Know Act (EPCRA)
                        Regulations (Sec. 313)            (800) 424-9346
                        Toxics Release Inventory data     (202) 260-1531
Air                   Clean Air Act                       (919) 541-0888
Solid Waste &         Comprehensive Environmental
 Emergency Response    Response, Compensation, and
                       Liability Act (Superfund)/
                      Resource Conservation and Recovery
                       Act / EPCRA (Sec. 302/304/311/312) (800) 424-9346
Water                 Clean Water Act                     (202) 260-7588

___________________________________________________________________________

               TABLE 5. OTHER FEDERAL OFFICE/OTHER GROUP  
              CONTACT NUMBERS FOR INFORMATION ON CHLORINE
________________________________________________________________________

Other Agency/Department/Group                            Contact Number
________________________________________________________________________
Agency of Toxic Substances & Disease Registry            (404) 639-6000
American Conference of Governmental Industrial Hygienists
   (Recommended Exposure Limit (see end note 5): 0.5 ppm)
   (Recommended Short Term Exposure Limit 
   (see end note 6):  1 ppm)                             (513) 742-2020
Consumer Product Safety Commission                       (301) 504-0994
Food & Drug Administration                               (301) 443-3170
National Institute for Occupational Safety & Health
Recommended Exposure Limit 
   (see end note 6):  0.5 ppm)                           (800) 356-4674
Occupational Safety & Health Administration
   (Permissible Exposure Limit (see end note 7): 1 ppm)
   (Check local phone book for phone number under Department of Labor)
________________________________________________________________________

VII. END NOTES

1. Standard Industrial Classification code is the statistical classifi-
cation standard for all Federal economic statistics.  The code provides 
a convenient way to reference economic data on industries of interest to 
the researcher.  SIC codes presented here are not intended to be an 
exhaustive listing; rather, the codes listed should provide an indication 
of where a chemical may be most likely to be found in commerce.

2. The RD50 concentration is that concentration that reduces respiratory
rate by 50%.

3. The RfD is an estimate (with uncertainty spanning perhaps an order of
magnitude) of the daily exposure level for the human population, including
sensitive subpopulations, that is likely to be without an appreciable risk
of deleterious effects during the time period of concern.

4. Calculated using the factor 2.9 mg/m3 (U.S. EPA 1989) to convert 1 ppm 
to 2.9 mg/m3 which is multiplied by 0.143 (the occupational standard 8-hour
breathing rate, 10 m3, divided by the assumed adult body weight, 70 kg, and
assuming 100% absorption) to obtain the dose in mg/kg/day (U.S. EPA 1988).

5.The ACGIH exposure limit is a time-weighted average (TWA) concentration
for an 8-hour workday for a 40-hour workweek.

6. This is a 15-minute short term exposure limit value that should not be
exceeded at any time.

7. This is a 15-minute ceiling exposure limit value that should not be
exceeded at any time.

VIII.  CITED REFERENCES

AQUIRE.  1994.  EPA ERL-Duluth's Aquatic Ecotoxicology Data Systems. U.S. 
EPA, Duluth, MN. Retrieved July 1994.

Budavari S, O'Neil MJ, Smith A, Heckelman PE (Eds.).  1989.  The Merck 
Index, 11th ed.  Merck & Co., Inc., Rahway, NJ, p. 954.

CHEMFATE.  1994.  Syracuse Research Corporation's Environmental Fate Data 
Bases.  Syracuse Research Corporation, Syracuse, NY.

HSDB.  1994.  Hazardous Substances Data Bank.  MEDLARS Online Information 
Retrieval System, National Library of Medicine.  Retrieved June, 1994.

NTP.  1992.  National Toxicology Program.  Toxicology and Carcinogenesis 
Studies of Chlorinated Water (CAS NOS. 7782-50-5 and 7681-52-9) and 
Chloraminated Water (CAS No. 10599-90-3) (Deionized and Charcoal-Filtered) 
in F344/N Rats and B6C3F1 Mice (Drinking Water Studies).  U.S. Dept. of 
Health and Human Services, National Institutes of Health, Research 
Triangle Park, NC.  NTP TR 392.

Seiler HG, Sigel H, Sigel A.  1988.  Handbook on Toxicity of Inorganic 
Compounds.  Marcel Dekker, Inc., New York, pp. 223-237.

Stokinger HE.  1981.  The halogens and the nonmetals boron and silicon.  
In:  Clayton GD, Clayton FE, Eds.  Patty's Industrial Hygiene and 
Toxicology, 3rd ed., Vol. 2B.  New York:  John Wiley & Sons, pp. 2954-2965.

TRI92.  1994.  Toxic Chemical Release Inventory.  National Library of 
Medicine, National Toxicology Program, Bethesda, MD.

U.S. EPA.  1985.  U.S. Environmental Protection Agency.  Ambient Water 
Quality Criteria for Chlorine - 1984.  Office of Water, Criteria and 
Standards Division, Washington, D.C.  EPA 440/5-84-030.

U.S. EPA.  1987.  U.S. Environmental Protection Agency.  Reportable 
Quantity Document for Chlorine.  First Draft.  Office of Solid Waste 
and Emergency Response, U.S. EPA, Cincinnati, OH. ECAO-CIN-R387.

U.S. EPA. 1988. U.S. Environmental Protection Agency. Methodology for 
Evaluating Potential Carcinogenicity in Support of Reportable Quantity 
Adjustments Pursuant to CERCLA Section 102. Carcinogen Assessment Group, 
Office of Health and Environmental Assessment, U.S. EPA, Washington, D.C., 
pp. 21, 22. OHEA-C-073.

U.S. EPA.  1989.  U.S. Environmental Protection Agency.  Drinking Water 
Criteria Document for Chlorine, Hypochlorous Acid and Hypochlorite Ion.  
Prepared for the Office of Drinking Water.  Prepared by Environmental 
Criteria and Assessment Office, U.S. EPA, Cincinnati, OH.

U.S. EPA.  1990.  U.S. Environmental Protection Agency.  Reportable 
Quantity Document for Chlorine, Draft.  Prepared by Chemical Hazard 
Evaluation and Communication Group, Oak Ridge National Laboratory.  
Environmental Criteria and Assessment Office, U.S. EPA, Cincinnati, OH.

U.S. EPA.  1994.  U.S. Environmental Protection Agency. Integrated Risk 
Information System (IRIS) Online.  Coversheet for Chlorine.  Office of 
Health and Environmental Assessment, U.S. EPA, Cincinnati, OH,  
Retrieved 7/94.

APPENDIX A.  SOURCES SEARCHED FOR FACT SHEET PREPARATION

AQUIRE. 1994. Aquatic Information Retrieval online data base. Chemical 
Information Systems, Inc., a  subsidiary of Fein-Marquart Assoc.

ATSDR.  1989-1994.  Agency for Toxic Substances and Disease Registry.  
Toxicological Profiles. Chamblee, GA: ATSDR.

Budavari S, O'Neil MJ, Smith A, Heckelman PE (Eds.).  1989.  The Merck 
Index, 11th ed.  Rahway, N.J.:  Merck & Co., Inc.

CHEMFATE.  1994.  Syracuse Research Corporation's Environmental Fate 
Data Bases.  Syracuse Research Corporation, Syracuse, NY.

Clayton GD, Clayton FE, Eds.  1981-1982.  Patty's Industrial Hygiene 
and Toxicology, 3rd ed.  New York:  John Wiley & Sons.

GENETOX. 1994. U.S. EPA GENETOX Program, computerized database. 

HSDB.  1994.  Hazardous Substances Data Bank.  MEDLARS Online Information 
Retrieval System, National Library of Medicine.

IARC. 1979-1994. International Agency for Research on Cancer.  IARC 
Monographs on the Evaluation of Carcinogenic Risk of Chemicals to Man. 
Lyon: IARC.

NIOSH (National Institute for Occupational Safety and Health).  1992.  
NIOSH Recommendations for Occupational Safety and Health.  Compendium of 
Policy Documents and Statements.  Cincinnati, OH: NIOSH.

NTP.  1994.  National Toxicology Program.  Toxicology and Carcinogenesis 
Studies.  Tech Rep Ser.

NTP.  1994.  National Toxicology Program.  Management Status Report.  
Produced from NTP Chemtrack system.  April 8, 1994.  National Toxicology 
Program, Research Triangle Park, NC. OSHA.  1994.  Occupational Safety 
and Health Administration.  Table Z-2.  Limits for Air Contaminants.

RTECS.  1994.  Registry of Toxic Effects of Chemical Substances.  MEDLARS 
Online Information Retrieval System, National Library of Medicine.

U.S. Air Force.  1989.  The Installation Restoration Toxicology Guide, 
Vols. 1-5.  Wright-Patterson Air Force Base, OH.

U.S. EPA (U.S. Environmental Protection Agency).  1991.  Table 302.4 List 
of Hazardous Substances and Reportable Quantities 40 CFR, part 
302.4:3-271.

U.S. EPA.  Most current.  Drinking Water Regulations and Health Advisories. 

Office of Drinking Water, U.S. Environmental Protection Agency, 
Washington, D.C.

U.S. EPA.  Most Current.  Health Effects Assessment Summary Tables.  
Cincinnati, OH: Environmental Criteria and Assessment Office, U.S.EPA.

U.S. EPA reviews such as Health and Environmental Effects Documents, 
Health and Environmental Effect Profiles, and Health and Environmental 
Assessments.

U.S. EPA.  1994.  Integrated Risk Information System (IRIS) Online.  
Cincinnati, OH:  Office of Health and Environmental Assessment.