Minnesota’s moose are inexplicably dying. A $1.2 million study was set in motion to determine why. In February, the Minnesota Department of Natural Resources (DNR) released its moose survey. A Star Tribune headline summed it up: “State moose population dives by a third in annual count.” The DNR called off the moose hunt indefinitely.
Global warming was blamed. But, according to the Natural Resources Research Institute, global warming alone is too simplistic an explanation. Moose are moving into areas of North Dakota where temperatures are warmer than Minnesota’s.
Consider the possibility that a clue to solving the “mystery of the disappearing moose” is sulfates. Several biologists have told me they agree the theory warrants research.
Sulfates and PEM
A moose is a ruminant. Cattle, another ruminant, have long been plagued with high-sulfate induced Polioencephalomalacia (PEM). Ruminants that ingest too much sulfur (as sulfate) from food and water may end up with PEM. The result is neurological displays of erratic behavior and sudden death. Especially vulnerable are lactating cows and young animals, which may correlate with moose losses in northeastern Minnesota.
Symptoms of PEM are nearly identical to those caused by brain worm; so far, though suspected, not many moose deaths have been diagnosed as brain worm. Also, PEM can induce copper deficiency, which has been found in Minnesota moose.
All ruminants have sulfate-reducing bacteria in their rumen. The rumen is anaerobic, with a pH between 5.5 and 7.2. Sulfates reduced by rumen bacteria produce hydrogen sulfide.
In our waters, sulfates trigger sulfate-reducing bacteria in anaerobic sediments, producing hydrogen sulfide and methylmercury. Hydrogen sulfide damages wild rice.
Basically, a moose does the same thing in its rumen that occurs in the anaerobic sediments of our waters. Production of too much hydrogen sulfide could result in PEM. It does not take much to do it. In cattle, total sulfate levels in feed (dry matter) plus water intake amounting to 0.4% (.004), 0.26% (.0026) for lactating cows.
“Normally sulfate in the animal’s diet is utilized by rumen bacteria to produce bacterial protein,” writes Dr. Tony Knight of the University of Colorado. “Excess sulfate (SO4) intake in ruminants results in the over-production of hydrogen sulfide by the rumen microflora. This highly toxic gas (H2S) is inhaled when the animal eructates and is absorbed into the blood stream via the lungs. The sulfides inhibit cytochrome C. oxidase, a critical enzyme in the electron transport system of cells. Consequently, the brain that is highly dependent on energy metabolism, is energy deprived and undergoes malacia or softening, the main component of PEM.”
In addition, “hydrogen sulfide is absorbed across the rumen wall into the blood stream. … Sulfide interferes with energy production much in the same way that cyanide does.” (Iowa University)
The University of Delaware’s, “High Sulfate Induced Polioencephalomalacia (PEM) in cattle – burping can be dangerous if you are a ruminant,” concluded, “… Because H2S is so toxic, damage to lung tissue could predispose animals to secondary bacterial or viral infections even if clinical symptoms of PEM do not exist.”
In February, biologists of the Grand Portage Band of Minnesota Chippewa found that the first mortality of its collared moose study had pneumonia, making it vulnerable to predators.
Moose may have a built-in mercury methylation factory
Sulfate-reducing bacteria in a moose’s anaerobic rumen not only convert sulfates to hydrogen sulfide, it appears they could also convert mercury to methylmercury. If mercury is present, mercury methylation could occur within the rumen. All that cellulose floating around inside a moose rumen is a source of reactive carbon, another necessary component of mercury methylation.
We may have moose in Minnesota ingesting sulfates and mercury into their own rumen methylation factory, possibly producing both excess hydrogen sulfide and methylmercury – a double whammy of neurotoxins.
We know that methylmercury can cross mammal membrane barriers including placental and blood-brain barriers. Just as methylmercury affects the brains of our children, so too could it affect Minnesota’s moose.
What if hydrogen sulfide gas and methylmercury, together or singly, enter the respiratory tract of Minnesota’s moose? What if hydrogen sulfide and methylmercury are absorbed to enter the bloodstream? What if either one, or both simultaneously, crosses the blood-brain barrier? Impairment? Incapacitation? Death?
Moose are what they eat, or drink
Sulfate levels in Minnesota waters are increasing due to anthropogenic activities.
Water plants (macrophytes) that moose eat grow in anaerobic sediments; often sulfate rich “hot spots.” Many plants uptake sulfate, mercury, and/or methylmercury. The University of Wisconsin, and the San Jose State University Research Foundation, have respective studies showing that wild rice uptakes mercury and methylmercury.
During the spring and summer moose consume 40-70 pounds per day of aquatic and terrestrial vegetation, increasing their body weight 25 percent. As much as half their total diet is aquatic macrophytes. And “a moose can store more than 100 pounds of food in its stomach,” according to the DNR.
Macrophytes also contain sodium, which moose need — especially lactating cows. But macrophytes thrive in “slow streams, small lakes with mucky bottoms, and beaver ponds,” anaerobic areas where sulfates and mercury would be most concentrated. Mineral licks are another source of sodium, and sulfate, where moose drink “copious” amounts of water.
How high are sulfate levels in sediments, in aquatic and terrestrial plants, and in water sources? How high are mercury and methylmercury levels?
Sulfite, also produced during reduction in the rumen, “is absorbed, oxidized to sulfate and then recycled back to the rumen available to be reduced again” (University of Delaware). What happens to Minnesota’s moose if methylmercury is also triggered and retriggered by sulfate reduction in the rumen?
Do moose cows pass a mercury burden to their calves? In northeastern Minnesota, past moose studies by the Fond du Lac Ojibwe Band and the DNR have found high cow mortality rates and low calf survival.
Climate change and heat stressed moose
As temperatures climb, moose spend more time in anaerobic-sulfate-laced sediments, staying cool, eating more aquatic plants. Warm weather increases activity of sulfate-reducing bacteria, increasing mercury methylation. Sulfate concentrations in mineral licks and water sources intensify through evaporation, particularly during drought with reduced moisture recharge.
Moose normally drink large amounts of water, in warm weather they drink even more; lactating cows drink more yet. Moose consumption records lacking, “Cattle may drink more than 2 gals. of water/100 lbs. of body weight when temperatures exceed 80° F, more than twice the intake of a 1,000-lb. animal at a temperature of 40° F.” (Protect your herd from high-sulfate water) Twice as much water, twice as much sulfate.
If moose were already toxin stressed, additional heat stress would be overwhelming. Too hot, and they may stop eating. However, moose that “simply tipped over” have died with full stomachs and yet were malnourished. Why?
When winter hits, are moose only facing stress from weather and the search for food – difficult enough – or are they already weakened from an insidious battle with toxins that began months earlier? Are sulfates the underlying driver?
Minnesota should replace the hunting season on our moose with a hunting season on sulfates. Until we have answers, Minnesota’s moose must be placed on the endangered species list. Before we conclude that there is nothing we can do to halt the “precipitous” decline of Minnesota’s moose, we need to find out just what is killing them. It may be us.
C.A. Arneson lives on a lake in the Ely area.
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