Ozonation Effects on the Speciation of Dissolved Iodine in Artificial Seawater at the National Aquarium in Baltimore
IAAAM 2000
Johanna Sherrill1, DVM, MS; Brent Whitaker2, MS, DVM; George T.F. Wong3, PhD
1Smithsonian National Zoological Park, Department of Animal Health, Washington, DC, USA; 2National Aquarium in Baltimore, Department of Animal Health, Baltimore, MD, USA; 3Old Dominion University, Department of Ocean, Earth and Atmospheric Sciences, Norfolk, VA, USA

Abstract

Numerous studies and reviews have been conducted on the control, regulation, and functions of thyroid tissue in fish.2,4,5,7 In both bony and cartilaginous fishes, thyroid metabolism is affected by dietary and environmental iodine levels.3,7,10 In fish, absorption of iodine from the aqueous environment, via diffusion across the gill membranes, is considered to be more efficient than absorption from the alimentary tract.10 In fish and other vertebrates, low levels of environmental iodine and goitrogenic substances (e.g., ammonia, nitrates, nitrites, urea, chemical toxins) have been associated with the development of thyroid lesions, specifically hyperplasia (goiter)3,6,8,9 and neoplasia (e.g., adenomas, adenocarcinomas).8-10

As a trace element in the marine environment, iodine occurs in several forms due to ongoing oxidative processes. In seawater, total dissolved iodine consists of two inorganic chemical species, iodide (I -) and iodate (IO3-), plus dissolved organic iodine (DOI).11,12 Iodide is required for synthesis of the thyroid hormones tri-iodothyronine (T3) and thyroxine (T4) in vertebrates, including fish.2,5,7 Large aquarium systems, however, often use ozone, a strong oxidant, in order to remove organic debris, including bacteria and viruses, from tank water.1 It is likely that ozone treatment in aquaria also alters the speciation and thus the bio-availability of dissolved iodine in artificial seawater, with subsequent effects on iodine metabolism and thyroid health in fish.

The primary goal of our study was to examine the effects of ozonation on the speciation of dissolved iodine in artificial seawater made at the National Aquarium in Baltimore (NAIB). The effect of adding ozone to seawater is measurable in millivolts (mV) as oxidation-reduction potential (ORP). We hypothesized that ozone concentrations required to achieve ORP levels approximating those in an ozone contact chamber (800 mV) and protein skimmer (400 mV) would significantly change iodine species concentration in artificial seawater, resulting in a relative iodine deficiency for resident fish. Because the NAIB Atlantic Coral Reef exhibit tank (ACR), a closed, ozonated 1.3 x 106 L (335,000-gallon) system, has a low-grade incidence of thyroid lesions in its fishes (e.g., thyroiditis, hyperplasia, adenoma, adenocarcinoma), the secondary goal of our study was to examine iodine levels present in the ACR and any possible correlations with thyroid disease.

A laboratory experiment was performed which compared iodine speciation of aliquots of 25.5°C NAIB raw seawater mix before, during, and after exposure for fixed time periods to air only, or to concentrations of ozone needed to achieve an ORP of 400 mV or 800 mV. Aliquots were immediately frozen at -20°C until analyzed. Differential pulse polarography and cathodic stripping square wave voltammetry,12 both electrochemical methods, were used to detect levels of I -and IO3-, respectively, in each sample. Total dissolved iodine was measured separately according to other recently developed methods,12 allowing calculation of DOI as the difference between total dissolved iodine and total inorganic iodine (I-+ IO3-).11,12 Results revealed a systematic decrease in concentrations of I- and DOI and concomitant increase of IO3-with increasing exposure to ozone. At an ORP of 800 mV, approximately two-thirds of the initial I -disappeared, DOI became undetectable, and there was no significant change in the concentration of total iodine. This suggests an ozone-induced conversion of I -to IO3-and a conversion of -DOI to I -and/or IO3. Additionally, ACR water samples were found to be virtually free of I-and DOI.

Based on these findings, we conclude that ozonation of artificial seawater may alter the relative concentrations of iodine species present in a closed tank system. Furthermore, it is possible that depletion of I- and DOI via oxidation by ozone and/or biologic processes is linked to thyroid disease documented in ACR fish over recent years. Thus, it may be advisable to supplement the diet and/or tank water of captive teleosts and elasmobranchs living in ozonated seawater with iodide. Iodide concentrations ranging from 0.1-0.15 µM the tank water may prevent goiter in several species of elasmobranchs housed in marine aquaria.3 Ideally, frequent testing of tank water for I -, IO3-, and total dissolved iodine levels is recommended to detect fluctuations in available iodine and aid in calculation of appropriate supplement dosages for resident fish. Concentrations of phytoplankton and organic debris, temperature, pH, and other factors are also reported to affect iodine speciation in artificial and natural seawater systems.3,11,12 Some of these factors, as well as the presence of possible goitrogens or thyrotoxins, may be examined in future investigations.

Acknowledgments

The authors wish to thank the generous staff at the National Aquarium in Baltimore, especially Ryan Bromwell, April Smith, Jill Arnold, Liz Neely, and Andy Aiken (technical support); Susie Ridenour (library services); Valerie Lounsbury (editorial input); Michele Martin, and Ian Walker (animal health). Financial support for iodine analyses was granted through the NAIB Biological Programs Department.

References

1.  Aiken A. 1995. Use of ozone to improve water quality in aquatic exhibits. Int. Zoo. Yb. 34:106-114.

2.  Bonga SEW. 1993. Endocrinology. In: Evans, D.H. (ed.) The Physiology of Fishes. CRC Press, Inc., Boca Raton, Florida, Pp. 469-502.

3.  Crow GL, MJ Atkinson, B Ron, S Atkinson, AD Skillman, GTF Wong. 1998. Relationship of water chemistry to serum thyroid hormones in captive sharks with goiters. Aquatic Geochem. 4:469-480.

4.  Eales JG, SB Brown. 1993. Measurement and regulation of thyroidal status in teleost fish. Rev. Fish Biol. Fish. 33:299-347.

5.  Gorbman A. 1969. Thyroid function and its control in fishes. In: Hoar, W.S. and Randall, D.J. (eds.) Fish Physiology (II) Endocrinology. Academic Press, Inc., New York, New York, Pp. 241-274.

6.  Hoover KL. 1984. Hyperplastic thyroid lesions in fish. Natl. Cancer Inst. Monogr. 65:275-289.

7.  Leatherland JF. 1994. Reflections on the thyroidology of fishes: from molecules to humankind. Guelph Ichthyol. Rev. 2:1-68.

8.  Nigrelli RF, GD Ruggieri. 1973. Hyperplasia and neoplasia of the thyroid in marine fishes. Mt. Sinai J. Med. 41:283-93.

9.  Spotte S. 1992. Captive Seawater Fishes. John Wiley and Sons, Inc., New York, New York.

10. Stoskopf MK. (ed.). 1993. Fish Medicine. W.B. Saunders Company, Philadelphia, Pennsylvania.

11. Wong GTF. 1991. The marine geochemistry of iodine. Rev. Aquatic Sci. 4(1):45-73.

12. Wong GTF, XH Cheng. 1998. Dissolved organic iodine in marine waters: determination, occurrence and analytical implications. Mar. Chem. 59(3-4):271-281.

Speaker Information
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Johanna Sherrill, DVM, MS
Department of Research and Veterinary Services
Mystic Aquarium


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