In case anyone forgets the relationship between energy costs and the costs of commercial fertilizer ingredients, here’s a refresher: The process starts when natural gas (methane) is blended with water. Once the two combine, they’re subjected to high temperature and extreme pressure. The resulting chemical reaction yields carbon dioxide gas (CO2) and hydrogen (H) gas. Nitrogen (N) is then removed from Earth’s atmosphere (which is 78% N). The N extracted from air is blended with the isolated H gas under high temperature and pressure. Thus merged, one N and three Hs react chemically, becoming one anhydrous ammonia (NH3) molecule. Add the right amount of CO2 to the ammonia molecule – along with heat and pressure – and the result is urea. When natural gas prices increase, N costs rapidly do likewise.
Early January ammonia price (FOB Tampa) weighed in at $1,014/ton, an increase, within the previous 30 days, of $114/ton. The phosphates (both diammonium and monoammonium) have not increased in price, due to limited buying.
China’s terminating fertilizer exports further tightens world urea supplies, such that U.S.-produced urea value remains at least $90/ton below rest-of-world levels. U.S. growers hoping for lower urea prices by planting time are disappointed to learn that three N production plants in China’s Shanxi province have been directed to cut their capacity to 50% due to pollution abatement efforts preceding the Winter Olympics. It’s highly likely that more Chinese urea factories could be asked to stifle production. According to Bloomberg Intelligence Analyst Alexis Maxwell, “Chinese exportable supply is firmly out of the market through May.” While ethanol does not substitute directly for natural gas as an energy source, higher methane prices encourage increased production of ethanol. Projected U.S. 2022 ethanol corn demand was raised 75 million bushels to 5.325 billion bushels. This means that more corn-based distillers’ grains will hit the cattle feed market. That fact has livestock health implications.
Gene Schmitz, University of Missouri Extension livestock specialist, said there are definite pluses for feeding distillers’ dried grains (DDGs). The biggest plus is that DDGs contain crude protein, concentrated to roughly three times the level found in shell corn (DDGs have between 25% and 35% crude protein). The second plus is their energy value: with the removal of starch from kernels, the energy comes primarily from oil and digestible fiber. Thirdly, DDGs are a good source of phosphorus – good enough to reduce or eliminate the need for phosphorus supplementation. But Schmidt cited one major negative: Not all DDGs are the same.
The nutrient composition of this feedstuff varies by ethanol plant. His biggest concern is that sulfur (S) toxicity is possible. In DDGs, sulfur ranges from 0.35% – 1.4%, which can potentially cause health concerns in beeves. Cattle have a nutrient requirement for S of 0.15% dry matter, with a maximum tolerable ceiling of 0.4%. Sulfur toxicity signs include decreased feed intake and slow or stunted growth. Producers must consider all S sources offered to cattle before introducing DDGs into their diets. If dietary S levels drift above 0.15%, the formation of the amino acids methionine and cysteine becomes restricted, which undermines protein synthesis. The reason behind some DDGs containing a lot more S is the degree to which sulfuric acid is employed at ethanol plants in liberating starch from corn kernels. That acid is used much more aggressively in producing fuel-destined ethanol compared to ethanol destined for whiskey. Least-cost grain ration formulations will draw in more DDGs, usually without consideration for potentially harmful S levels.
Bovine polio-encephalomalacia (PEM), first reported in 1956, was described as a neurologic disorder of cattle characterized by blindness, ataxia (loss of balance), recumbency (failure to stand) and seizures. PEM was once thought to be caused exclusively by thiamine deficiencies. The deficiency was thought to develop because the rumen did not produce enough thiamine, or because products like amprolium (a coccidiostat) inhibited thiamine production. We now know that PEM, diagnosed in the brain, can be caused by S toxicity, in addition to lead toxicity, salt toxicity and hypoxia as well as thiamine deficiency. Sulfur toxicity does respond to thiamine treatment but is not caused by a thiamine deficiency. Increasingly, PEM is caused by S toxicity.
When excess S is ingested, rumen microbes produce too much hydrogen sulfide. This compound is absorbed across the rumen wall into the bloodstream. Elevated serum sulfide impedes cellular energy production. Since the brain has a high energy requirement, high sulfides seriously impair its performance. Sulfide interferes with energy production in much the same way as cyanide. Sulfur intake occurs through water, as well as in feed, so the total dietary intake of S is needed to evaluate the risk of PEM. This is especially pertinent in feedlots now because of increasingly universal ethanol byproducts, especially DDG with solubles (DDGS). Ethanol byproducts may contain a high concentration of S. When cattle are transitioning to high S intake conditions, the ruminal sulfide concentration peaks one to three weeks after the change.
Not all cattle consuming over 0.4% dietary S will develop clinical PEM. Factors like ruminal microbial populations, trace element concentration or ruminal pH can affect S production and absorption. Insoluble metal sulfides of copper, iron or zinc could decrease the availability of sulfide. As pH decreases, the amount of hydrogen sulfide in the ruminal gas cap increases. Sulfur-associated PEM occurs in two forms. The acute form is characterized by blindness, recumbency, seizures and death. The subacute form is characterized by visual impairment and ataxia. Twitching of the ears or facial muscles is frequently observed. The subacute form is frequently followed by recovery with minor neurologic impairment.
In suspected PEM cases, it’s important to analyze water and feed for S levels. There is much variability in the S content from ethanol byproducts, both within an ethanol factory and between factories. Thus, periodic sampling should be conducted to have an accurate idea of dietary intake of S. There is no specific treatment for PEM; treatment is supportive. When animals go off feed with PEM, production of sulfide ceases and this is one reason that subacutely affected animals usually recover without treatment. Removal of animals from expected excessive S sources is the best control measure. Test complete cattle rations to make sure S doesn’t exceed 0.4% on dry matter basis. Let’s not allow the craziness of the energy and fertilizer markets to undermine ruminant health.
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