In September 1982, a Charlottesville, Virginia, dentist reported treating two women, one 17 and one 28 years old, for dental enamel erosion. Both exhibited general erosion of enamel from the anterior surfaces of the incisors and premolars, clinically consistent with exposure to acid (1,2). Neither had any history of unusual occupational, dietary, or medical exposures to acid. However, both were competitive swimmers who trained regularly at the same private club pool.

To identify any additional cases, a questionnaire was mailed to all club-member households. A total of 747 members responded to the survey. Club members were considered to have symptoms compatible with enamel erosion if, during the summer of 1982, they reported having one or more of the following symptoms "a lot" or two or more of these symptoms "sometimes": 1) gritty or rough teeth; 2) transparent or yellow teeth; 3) "chalky" white teeth; 4) painful teeth when chewing. Members were also considered cases if their dentists had clinically diagnosed enamel erosion during or after the summer of 1982.

Of the 452 frequent swimmers,* 69 (15%) reported symptoms compatible with enamel erosion, compared to nine (3%) of 295 infrequent or nonswimmers (p 0.001). In addition, of 59 members of a swim team, 23 (39%) met the case definition, compared to 12% (46/393) of all other frequent swimmers (p 0.001). A second questionnaire was sent to all 452 frequent swimmers and was returned by 294 (65%). Of the 132 persons who swam 5 or more days per week, 35 (27%) were cases, compared to 14 (9%) of 162 persons who swam less than 5 days per week (p 0.001).

An oral pathologist examined 30 individuals who met the case definition and 60 control swimmers matched for age, race, and sex. Four (13%) of 30 cases had clinically evident general enamel erosion, compared to none of 60 controls (p = 0.005). Each of these four trained regularly in the pool for competitive swimming meets, compared to one of eight matched controls (p = 0.01). The four patients with clinically evident erosion did not differ significantly from controls with respect to history of occupational, dietary, and medical exposures to acid.

A water sample, obtained from the pool in September by one of the swimmers and tested by Virginia's Consolidated State Laboratories, exhibited no buffering capacity and a pH of 2.7, i.e., an acid concentration approximately 100,000 times that recommended for swimming pools (3). State health department epidemiologists were unable to obtain additional samples directly from the pool because it had been drained at the conclusion of the swimming season.

Site inspection in November by the Virginia State Department of Health revealed a gas-chlorinated pool with corrosion of metal fixtures and marked etching of unpainted cement exposed to the pool water. A review of pool management practices revealed the water was usually tested each morning for pH and the level of free chlorine. Soda ash (Na((2))CO((3))) was added to neutralize the acid when a standard colorimetric phenol red pH indicator (pH range 6.8-8.2) indicated the water was acidic. The manager did not report that the pool water was rechecked to verify that the pH had been brought up into the accepted range for swimming pools (pH 7.2-7.8) (4). No records were kept either of the daily readings of free chlorine levels and pH or of the daily use of chlorine gas and soda ash. According to the pool manager, the pH indicator kit commonly registered a pH of 6.8 during the 1982 season. Reported by RA Prindle, MD, Charlottesville Health Dept; RP Elzay, DDS, Medical College of Virginia; CW Armstrong, MD, LS Funkhouser, MD, GB Miller, Jr, MD, State Epidemiologist, Virginia State Dept of Health; Field Svcs Div, Epidemiology Program Office, CDC.

Editorial Note

Editorial Note: Large pools are sometimes chlorinated with chlorine gas (Cl((2))), instead of hypochlorite, because of the economic advantages (5). Unlike hypochlorite, gas chlorination causes pool water to become acidic because chlorine gas reacts with water to form hydrochloric acid (HCl): Cl((2)) + H((2))O --- HOCl + HCl. Hypochlorous acid (HOCl) is the germicidal agent in chlorination; HCl is an unwanted byproduct. Excess acidity is commonly neutralized and gas (Cl((2))), instead of hypochlorite, because of the economic advantages (5). Unlike hypochlorite, gas chlorination causes pool water to become acidic because chlorine gas reacts with water to form hydrochloric acid (HCl): Cl((2)) + H((2))O --- HOCl + HCl. Hypochlorous acid (HOCl) is the germicidal agent in chlorination; HCl is an unwanted byproduct. Excess acidity is commonly neutralized and buffered by the addition of soda ash.

Tooth enamel does not decalcify in acidic solutions unless the pH is below 6.0 (6). Even at a pH between 5 and 6, hours of cumulative exposure are required for clinically evident decalcification to occur (6). With proper buffering to maintain a recommended pool pH (pH 7.2-7.8) (4), gas-chlorinated pools operate with a substantial margin of safety as regards enamel erosion. However, if a gas-chlorinated pool becomes inadequately buffered through the addition of inadequate quantities of soda ash, the pH may decrease rapidly--in one observed instance, from a pH of 7.4 to approximately 4.0 overnight (5).

General enamel erosion has been observed among industrial workers exposed to acid fumes (1) and among people consuming excessive quantities of acidic fruit, beverages, and medication (2). In 1980, an outbreak of enamel erosion similar to the present one was investigated at a gas-chlorinated public pool in New Jersey. The swimming pool water was epidemiologically implicated as the cause, but the mechanism could not be determined (7). In the present outbreak, the epidemiologic evidence showed that prolonged exposure to the pool water was associated with enamel erosion and that, on at least one occasion, the water was far below the recommended pH. These findings, plus the apparently inadequate maintenance practices, implicated the pool water as the cause of the enamel erosion.

The American Public Health Association recommends that proper pool maintenance records be kept, including thrice-daily chlorine levels and pH readings, as well as the daily use of chlorine gas and soda ash (3). Since, with a standard phenol red indicator system (pH range 6.8-8.2), any pool water sample with a pH below 6.8 will read as pH 6.8, the person testing the water should take into account the accuracy of the colorimetric pH indicator. If the phenol red indicator shows pH 6.8, the pool should be promptly corrected to pH 7.2 or above and so verified.

References

1. Bruggen Cate HF. Dental erosion in industry. Br J Ind Med 1968;25:249-66.

2. Stafne EL, Loestadt SA. Dissolution of tooth substances by lemon juice, acid beverages, and acids from other sources. J Am Dent Assoc 1947;34:586-92.

3. American Public Health Association. Public swimming pools: recommended regulations for design and construction, operation and maintenance. Washington, D.C.: American Public Health Association, 1981.

4. Center for Environmental Health. Swimming pools--safety and disease control through proper design and operation. Atlanta, Georgia: Centers for Disease Control, Department of Health and Human Services, March 1983.

5. White GC. Handbook of chlorination. New York: Van Nostrand Reinhold Company 1972:466-526.

6. McClelland JR. The decalcification of human tooth enamel. Dental Cosmos 1926;68:127-32.

7. Savad EN. Enamel erosion ... multiple cases with a common cause (?). J New Jersey Dent Assoc 1982;53:32-7, 60.

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