Back to Leopold Letter Fall 1999
By PETER WEYER, Associate director, Center for Health Effects of Environmental Contamination, University of Iowa
EDITOR'S NOTE: Reports last spring of record nitrate levels in the Raccoon River, as well as growing concerns about groundwater contamination by nitrogen fertilizer, livestock manure, sewage systems and septic tanks, prompt another look at the safety of Iowa's rivers, lakes and reservoirs. At the heart of the discussion is the assumption that high concentrations of nitrate can be harmful to humans. But are they? Some say no.
To look at the science behind the debate, we called upon Peter Weyer, associate director of the Center for Health Effects of Environmental Contamination (CHEEC), which, along with the Leopold Center, was created by the 1987 Groundwater Protection Act. Weyer has worked on numerous studies on possible links between nitrate and cancer.
The following article is based on the latest research on nitrate in drinking water and public health concerns. A list of references used for this report appears at the end of the article.
Nitrate levels in source water supplies fluctuate by season. Levels are usually higher in the spring after snowmelt, or following heavy rainfall. Nitrate occurs naturally and has many sources including nitrogen fertilizers, crop residues, livestock waste, septic systems and organic matter from the soil.
Humans can be exposed to nitrate in a variety of ways. Nitrate is produced naturally in the human body. People ingest nitrate via drinking water and from a myriad of dietary sources including many vegetables (spinach is one of the largest accumulators of nitrate) and processed meats. Quantifying which sources have the biggest effects on the body has proven to be a daunting task. It is not nitrate per se that is a health concern, rather nitrite and N-nitroso compounds (NOCs).
Nitrite and NOCs are produced by a series of complex chemical reactions. In the human body, nitrate is turned into nitrite by the bacteria in saliva, the stomach or an infected bladder. Nitrite then reacts with certains substrates such as amines, amides and amino acids to produce NOCs, which have been found in numerous animal studies to be carcinogenic (U.S. Dept. of Health and Human Services 1998).
The historic area of concern with respect to nitrate exposure and human health is methemoglobinemia, or blue baby syndrome. Blue baby syndrome occurs when nitrite mediates the oxidation of the heme ion in hemoglobin (an oxygen-carrying protein pigment in red blood cells) to form methemoglobin. This can result in anemic hypoxia (oxygen-deficient blood), which can be life-threatening for an infant.
Because nitrate reduces to nitrite, there has been a longstanding concern about potential sources of nitrate, particularly in tap and well water used for infant formula. However, blue baby syndrome has been rarely diagnosed in the United States in recent years.
In the July 1999 issue of the journal Environmental Health Perspectives, Alex Avery of the Hudson Institute argues that evidence from clinical evaluation of 40 years of blue baby syndrome cases indicates that environmental sources of nitrate (particularly drinking water) may have little to do with development of the condition (Avery 1999a). He contends that gastrointestinal infection and related production of nitric oxide (which metabolizes to nitrite) may be the primary cause of many cases of blue baby syndrome. Avery concludes that the U.S. Environmental Protection Agency's 10 parts per million (ppm) limit for nitrate in drinking water is too stringent, and that the standard should be relaxed (see sidebar story that follows).
Avery takes his argument one step further in a June 24, 1999, Des Moines Register essay, and states that there is no proof that nitrate in drinking water poses a real threat for adults (Avery 1999b). He also questions the cost-benefit of nitrate removal processes in municipal drinking water treatment.
Let's assume that nitrate in drinking water does not contribute to the development of blue baby syndrome. Are there other human health concerns about long-term exposure to nitrate in water? Or are we overreacting to the presence of nitrate in our drinking water? Can an argument be made, from a public health standpoint, that it would be prudent to try and limit exposure to nitrate in drinking water?
The scientific literature includes many studies examining possible associations between nitrate in drinking water and chronic health problems. A few examples are:
With respect to cancer, there are numerous reports of epidemiological studies on drinking water nitrate and cancer risk, including:
While one can argue about the weaknesses and strengths of specific study designs, it is obvious that we cannot say for certain that nitrate in drinking water poses no potential problems for human health. The jury is still out, and further research is needed. In Iowa, we are currently studying nitrate in municipal drinking water and risk of a number of cancers. Researchers at the National Cancer Institute have ongoing studies of drinking water nitrate levels in the Midwest. Some of the problems we are faced with involve quantifying individual exposure levels to nitrate. Studies to date have used average municipal water supply levels as the exposure variable. Data are very scarce; in some cases, only a handful of values exist over a number of years.
Still, the question persists. Should the EPA raise the acceptable level for nitrate in drinking water at this time? Absolutely not. In Iowa and other Midwestern states where nitrate in water supplies is a common occurrence, public health safety demands we continue studying this, and common sense indicates EPA maintain the nitrate MCL at the current level.
The potential long-term health impacts and related costs to society could be staggering. Rather than relaxing the MCL, we should be working towards preventing contamination of water supplies by nitrate (whatever the source) as a prudent effort towards reducing potential risk to the public's health.
References
Arbuckle, T.E., G.J. Sherman, P.N. Corey, D. Walters, and B. Lo. 1988. Water nitrates and CNS birth defects: A population-based case-control study. Archives of Environmental Health 43(2):162-7.
Avery A.A. 1999a. Infantile methemoglobinemia: Reexamining the role of drinking water nitrates. Environmental Health Perspectives 107(7):583-86.
Avery A.A. 1999b. Dispel myths about the dangers of nitrates. The Des Moines Register, June 24, 1999.
Freedman, D.M., K.P. Cantor, M.H. Ward, and K.J. Helszsouer. Drinking water and non-Hodgkin's lymphoma: A population-based case-control study (abstract). Epidemiology 9(4 Suppl):S31.
Kostraba, J.N., E.C. Gay, M. Rewers, and R.F. Hamman. 1992. Nitrate levels in community drinking waters and risk of IDDM: An ecological analysis. Diabetes Care 15(11):1505-8.
LeClerc, H., P. Vincent, and P. Vandevenne. 1991. Nitrates in drinking water and cancer. Annales de Gastroenterologie et d Hepatologie 27(7):326-32.
Morales-Suarez, V.M., A. Llopis-Gonzalez, and M.L. Tejerizo-Perez. 1995. Impact of nitrates in drinking water on cancer mortality in Valencia, Spain. European Journal of Epidemiology 11(1):15-21.
Morales-Suarez, V.M., A.L. Llopis-Gonzalez, M.M. Tejerizo-Perez, and J. Ferrandiz-Ferrugud. 1993. Concentration of nitrates in drinking water and its relationship with bladder cancer. Journal of Environmental Pathology, Toxicology and Oncology 12(4):229-36.
Rademacher, J.J., T.B. Young, and M.S. Kanarek. 1992. Gastric cancer mortality and nitrate levels in Wisconsin drinking water. Archives of Environmental Health 47(4):292-4.
Rogers, M.A, T.L. Vaughan, S. Davis, and D.B. Thomas. 1995. Consumption of nitrate, nitrite, and nitrosodimethylamine and the risk of upper aerodigestive tract cancer. Cancer Epidemiology, Biomarkers and Prevention 4(1):29-36.
Seffner W. 1995. Natural water contents and endemic goiter - a review. Zantralblatt fur Hygiene und Umweltmedizin 196(5):381-98.
Tsezou, A., S. Kitsiou-Tzeli, A. Galla, D. Gourgiotis, J. Papageorgiou, S. Mitrou, P.A. Molybdas, and C. Sinaniotis. 1996. High nitrate content in drinking water: Cytogenetic effects in exposed children. Archives of Environmental Health 51(6):458-61.
U.S. Dept. of Health and Human Services, Public Health Service. 1998. National Toxicology Program, 8th Report on Carcinogens.
Van Maanen, J.M., A. van Dijk, K. Mulder, M.H. de Baets, P.C. Menheere, O. van der Heide, P.L. Mertens, and J.C. Kleinjans. 1994. Consumption of drinking water with high nitrate levels causes hypertrophy of the thyroid. Toxicology Letters 72(1):365-74.
Van Maanen, J.M., I.J. Welle, G. Hageman, J.W. Dallinga, P.L. Mertens, and J.C. Kleinjans. 1996. Nitrate contamination of drinking water: Relationship with HPRT variant frequency in lymphocyte DNA and urinary excretion of N-nitrosamines. Environmental Health Perspectives 104(5):522-8.
Ward, M.H., K.P. Cantor, A. Blair, and D. Riley. 1998. Nitrate from public water supplies and risk of non-Hodgkin's lymphoma in Iowa (abstract). Epidemiology 9(4 Suppl):S77.
Ward, M.H., S.D. Mark, K.P. Cantor, D.D. Weisenburger, A. Correa-Vilasenore, and S.H. Zahm. 1996. Drinking water nitrate and the risk of non-Hodgkin's lymphoma. Epidemiology 7(5):465-71.
Weisenburger, D. 1993. Potential health consequences of groundwater contamination of nitrates in Nebraska. Nebraska Medical Journal 78:7-10.
Back to Leopold Letter Fall 1999