Blue Baby Syndrome Q+A

In October of 2017, Canterbury medical officer of health Alistair Humphrey warned against rising nitrate levels in Christchurch’s private drinking wells, saying babies were at a health risk. Humphrey cited the 23% of wells in the area that had nitrate levels close to exceeding limits, saying that babies given feed mixed with water from these wells could develop methemoglobinaemia, otherwise known as blue baby syndrome.  This got people talking, and in the following months, numerous articles were published about the dangers of high-nitrate water, blaming agriculture (in particular dairy farming) for the issue. But was this really something to get worked up over? Let’s take a look at the condition, its history, and how much of a threat it really is to New Zealand’s infants.  

WHAT IS BLUE BABY SYNDROME? WHAT ARE ITS SYMPTOMS?

A succinct breakdown of how the condition operates is given by Jules Pretty and Gordon Conway in The Blue Baby Syndrome and Nitrogen Fertilizers:

“The body becomes progressively starved of oxygen, turning affected individuals blue, firstly around the lips, fingers, and toes and then spreading to the face and body. Under normal conditions haemoglobin in the blood passes through a well-balanced cycle of picking up oxygen in the lungs and releasing it to the body's tissues. But the process is disrupted if alternative oxidising agents are present. These combine with haemoglobin to form methaemoglobin, so preventing it from transporting oxygen. Nitrites, which are formed in the body from nitrates by the action of some bacteria, will oxidise haemoglobin in this way. When more than 5% of haemoglobin is converted to methaemoglobin, clinical symptoms of oxygen starvation begin to occur; by 30-40% the body is acutely short of oxygen, and at over 50% death usually occurs.

WHAT IS THE HISTORY OF THE CONDITION IN NEW ZEALAND?

Blue baby syndrome is in fact virtually non-existent in New Zealand’s medical history.

According to Alistair Humphry himself, there has only been a single case, and though he posits there may have been more, as the condition could be misdiagnosed as sudden infant death syndrome, those speculations remain merely that – speculation.

Most of the discussion centered around the disease in this country has been based on concerns over rising nitrate levels, which people warn ‘could’ cause methemoglobinemia.

These high nitrate levels, according to the numerous articles published on the subject over the past decade, are primarily the result of intensive agricultural activities.

WHEN WAS THE CONNECTION FIRST MADE BETWEEN NITRATES IN WATER AND BLUE BABY SYNDROME?

According to the article Blue Babies and Nitrate-Contaminated Well Water, published by the Wisconsin Department of Health and Family Services, the association between high nitrate levels in drinking water and the characteristic symptoms of blue baby syndrome was first made in the 1940s by Iowa Physician Hunter Comly.

Comly was treating two infants for cyanosis when he discovered both had been fed formulas diluted with water from shallow wells. The wells were tested, and their nitrate levels were found to be at 90 and 150 mg N/L.

From this, Comly hypothesised that high nitrate levels were decreasing the oxygen carrying capacity of haemoglobin in the babies. This lack of oxygenation caused lethargy, rapid heartrates, clubbed fingers and toes, irritability, developmental issues, and most notably, a bluish hue to the skin. Thus the term “blue baby syndrome” was born.

HOW DID THE U.S REACT?

In the wake of Comly’s initial discovery a nationwide survey was conducted to determine the frequency of methaemoglobinaemia occurrences.

This survey, which ran between 1949 and 1950, turned up a total of 278 cases, 39 of which resulted in death.

It was thus ordered by the American Public Health Association (APHA) that a limit be placed on nitrate levels in drinking water. Working with the World Health Organisation, they concluded that nitrate levels in water ingested by each of the 39 victims exceeded 10 parts per million.  So, a maximum contaminant level of 10 ppm nitrate-N was established across the United States.

WHAT DOES THE SCIENCE SAY?

In the decades since Comly first hypothesised the relationship between water nitrates and methemoglobinemia, a number of medical professionals and scientists have questioned its validity.

Perhaps the most prominent of these is James Avery, whose 1999 article Infantile Methemoglobinemia: Reexamining the Role of Drinking Water Nitrates reviewed historical cases and applied more current research to suggest that the allowed levels of nitrates in drinking water prescribed by the WHO were unnecessarily strict.

Avery theorized that diarrhoea and/or gastrointestinal infection/inflammation was the principal causative factor in infantile methemoglobinemia. He based this on the discovery that gastrointestinal disturbances can cause the condition in infants without exposure to high nitrate levels through water or food, and the fact that diarrhoea was a prominent symptom in the majority of drinking water linked cases. The key point for Avery was that (as mentioned in the description given by J. Pretty and G. Conway) it was nitrites not nitrates that were the actual cause of the condition. It was found that nitrates were converted into nitrites by bacteria formed in an irritated intestinal tract, and this explained the link between diarrhoea and methemoglobinemia.

Additionally, it had been found that protein intolerance accompanied by diarrhoea and/or vomiting could cause methemoglobinemia in infants less than 6 months of age without excessive intake of nitrates through food and water, and that, although over 90% of exogenous nitrate exposure comes from food, the only methemoglobinemia cases linked to food involved high levels of nitrite contamination. For example, a typical case involved carrot juice containing 775 ppm nitrite-N, which is over 700 times the MCL for nitrites.

According to Avery, “all of these observations strengthen[ed] the view that endogenous nitrite production, not exogenous nitrate contamination of drinking water, [was] the primary cause of methemoglobinemia.” It was his belief that scientists of 50 years previous had been misled by the presence of nitrates in water, which were simply a ‘red herring’ (Roger Smith, Dartmouth Medicine, 2000).

He further pushed this idea by pointing out that in the ten-year period between the WHO 1949-50 survey on blue baby syndrome and the eventual establishment of the 10-ppm limit in 1962, the number of reported cases dropped to almost nothing, despite the fact that no limits were in place during that time.

 In a 2014 article published on streamlinedenvironmental, New Zealand’s own Jim Cooke voiced his support of Avery’s theory, pointing out that, “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”, and saying it is important to note that the wells from which they drew the water were “poorly constructed and microbially polluted”, a fact that has been somewhat forgotten in recent years.

Cooke goes on to say that “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. He attributes this to a higher standard of well construction and greater awareness around avoiding microbial contamination. He also refers to a 2005 workgroup report  that shows a number of modern health experts to find the role of nitrate water in methaemoglobinaemia to be insignificant.

The report was produced by Mary H. Ward, Theo M. deKok, Patrick Levallois, Jean Brender, Gabriel Gulis, Bernard T. Nolan, and James VanDerslice, all leading professionals in fields ranging from Health and Human Services to Genetics. It discusses how human nitrogen production has increased rapidly since the 1950s, and (as of 2005) exceeds nitrogen fixed by natural sources by about 30%.

It would seem strange then that so few cases of blue baby syndrome have been reported in the past 30-40 years. Some would attribute that to the 10 mg/L limit, however, as the report points out, this level is generally met by public water supplies, but little is known about private wells, which are usually only monitored upon construction or when the property is old.

There are others still who have challenged the water nitrate/methemoglobinemia link, such as Lorna Fewtrell who conclusively stated in Drinking-Water Nitrate, Methemoglobinemia, and Global Burden of Disease: A Discussion (2004) that “no exposure–response relationship [can] be identified that relate[s] drinking-water nitrate levels to methemoglobinemia.” Or Aaron Hanukoglu and Pinhas Danon, who conducted a thorough study of endogenous methemoglobinemia associated with diarrhoeal disease in infants in 1996, and like Avery, found blue baby syndrome to be a more likely result of high-protein feeds and irritated intestinal tracts than drinking water with high levels of nitrates.

SO IS THERE CAUSE FOR CONCERN?

The concern around blue baby syndrome is perfectly understandable. The threat of any potentially life-threatening condition affecting infants will naturally be afforded a good deal of attention.

However, the more it is researched, the more likely it seems that Comly’s original theory regarding water nitrate levels is a flawed product of the limited scientific and health-based knowledge of the time.

With ever-growing awareness around microbial contamination, blue baby syndrome has become a thing of the past. According to American Scientist only two official cases have been reported in the states since the mid-1960s and none since 2000. In New Zealand, as previously stated, the disease has officially occurred only once, and in the UK, just a single case has been reported since the mid-1970s.

Whilst agricultural activities do have several negative flow-on effects in this country, the poor health of infants is certainly not one of them. It seems it’s time to put this topic to bed.

                     

                                                                         

 

                                                                           Works Cited 

     

Anderson, Henry, et al. "Blue Babies and Nitrate-Contaminated Well Water." Environmental Health Perspectives, vol.108, no.7, 2000, pp. 675-678. 

Avery, Alexander. "Infantile Methemoglobinemia: Reexamining the Role of Drinking Water Nitrates." Environmental Health Perspectives, vol. 107, no.7, 1999, pp. 583-586. 

Conway, Gordon and Jules Pretty. "The Blue Baby Syndrome and Nitrogen Fertilisers: A High Risk in the Tropics?" GATEKEEPER SERIES NO. 5. International Institute for Environment and Development. 

Cooke, Jim. "Nitrate pollution of drinking water: how big a health issue is it?" streamlined. Streamlined Environmental Ltd, March 24, 2014. Web. 5. June 3. 2018. 

Fewtrell, Lorna. "Drinking-Water Nitrate, Methemoglobinemia, and Global Burden of Disease: A Discussion." Environmental Health Perspectives, vol. 112, no.14, 2004, pp. 1371-1374. 

Smith, Roger. "The Blue Baby Syndromes: Did environment or infection cause a blood disorder in newborns?" American Scientist, vol. 97, no.2, 2017, pp. 94-96.