Reports of nitrate pollution of groundwater, with concentrations above the safe “New Zealand drinking water standard”, or World Health Organisation Guidelines, have been prominent in the media recently. This is particularly the case in Canterbury, where the Medical Officer of Health described rising nitrate levels as a “ticking time bomb”. Yet groundwater nitrate levels are rising all around the country, not just in Canterbury. This ought to pose questions for all New Zealanders with an interest in water quality. What is the basis for these “standards” or “guidelines”? And what is the evidence for human health effects at higher nitrate concentrations?
The basis for the guidelines
Our maximum acceptable value (MAV) for nitrate concentration in drinking water (11.3 mg/L nitrate-N) is based on the WHO Guideline Value (GV), which was established to protect infants from a condition commonly known as “blue baby syndrome”. Affected infants have an abnormally high amount of methaemoglobin in their blood, hence the condition’s scientific name, methaemoglobinaemia. Unlike regular haemoglobin, methaemoglobin (pronounced met-haemoglobin) cannot transport oxygen in the bloodstream. If too much of our blood’s haemoglobin becomes methaemoglobin, the result can be severe oxygen depletion in tissues and a bluish tinge to the skin. We all have some methaemoglobin in our blood, but certain substances can cause those levels to rise rapidly, especially in infants. For many years it was thought that nitrate was one such substance.
The origin of the guidelines
The origins of this view can be traced back to a paper published in 1945 by Hunter Comly, a physician in the mid-West of the US, who described blue-baby like symptoms in two infants who had ingested nitrate-rich well-water. A large number of similar papers followed, culminating in a review by Walton (1951) on behalf of the American Public Health Association, in which he considered some 270 cases of infant methaemoglobinaemia. Walton noted that no cases were observed when the drinking water’s nitrate concentrations were less than 10 mg/L NO3-N. To cut a long story short, this analysis became the basis for the WHO Guideline Value.
But was nitrate the sole culprit? Recent reviews of these original papers noted that both Comly and Walton commented on factors other than nitrate that may affect the development of infant methaemoglobinaemia. In particular, those authors observed that the condition was often accompanied by diarrhoea, and that the water in question was drawn from wells that were poorly constructed and microbially polluted. Over time, however, the subtleties of these earlier studies came to be overlooked, and a simple role for nitrate became accepted. This is a shame, because such a simple role is not supported by physiological evidence. Nitrate (NO3-N) per se doesn’t have the ability to transform haemoglobin into methaemoglobin. Nitrite (NO2-), nitrate’s close chemical cousin, does have this ability. Nitrate is reduced to the less stable nitrite by a specific group of bacteria under certain conditions, but such conditions do not generally occur in the human gut. On the other hand, water that is faecally contaminated, as was the case in the studies by Comly and Walton, may provide ideal conditions for the reduction of nitrate to nitrite.
Microbial contamination a co-factor
In the mid 20th century, infant methaemoglobinaemia was regularly reported in the United States, but today it is a rarity, despite increasing exposure to high-nitrate drinking water. The best explanations for this apparent anomaly are higher standards of well construction and greater awareness of the importance of avoiding microbial contamination. This also explains why the incidence in most developed countries (including New Zealand) is now very low, whereas in developing countries it is still relatively common. There is now consensus amongst health experts that the role of nitrate exposure in causing infant methaemoglobinaemia is minor and not a sound justification for the present nitrate standard for drinking water. Despite this reasonably unequivocal stance, the WHO retains the 50 mg/L nitrate (11.3 mg/L NO3-N) GV for infant methaemoglobinaemia. While this may appear an extremely conservative stance, it must be remembered that WHO Guidelines apply to the whole world, not just part of it that has microbiologically safe drinking water. Tellingly, though, the notes accompanying the Guidelines state that bottle-fed infants can consume up to 100 mg/l (equivalent to 22.6 mg/L nitrate-N) provided the water is microbiologically safe. This effectively doubles the concentration of nitrate that can be safely consumed provided the microbiologically safe condition is attained.
The strong evidence for microbial contamination being at least a cofactor in infant methaemoglobinaemia appears to have vanished under the radar in New Zealand. Risk maps have been developed, emphasising that the health risks of high nitrate in groundwater are confined to relatively small areas, but the linkage with microbial contamination is not included. In my view this omission is unfortunate because families taking drinking water from wells in the high-risk zone may be unduly concerned if their water is otherwise microbiologically safe. And the key message for concerned consumers of rural groundwater? Ensuring that drinking-water wells are of appropriate depth, properly constructed, and that well heads are sealed will not only reduce the risks of infant methaemoglobinaemia to near zero, but will also minimise the risks of contracting potentially serious illnesses from organisms such as Campylobacter and pathogenic E coli.
This blog is based on a review entitled “Are rising nitrate levels in rural groundwater a public health concern?” published in “Water” published by Water NZ, March 2014