Mitigating methane emission from livestock with ozone-degrading halomethanes. Are we moving too fast or too slow?

Disclaimer: This blog post is a primer intended for scientists and policymakers with an interest in limiting methane emissions from cattle. My qualifications are that I am a microbiologist with expertise in microbial metabolism. I have studied microbial metabolisms, authored a review on the biogeochemistry of chlorine, and obtained my Ph.D. in a laboratory studying chemical inhibitors of metabolism. I am not an authority on business/investments/law/animal husbandry and my analysis of any companies mentioned here should not the basis of any business/investment/legal/animal husbandry decisions.

Humanity has a methane-from-cattle problem. Our herd of 1 billion cattle is over 8 times the weight of all wild animals. In the United States, our herd size hovers about 100 million cattle. Cattle, like other ruminants including sheep, have an extra stomach full of microorganisms, called a rumen. The microorganisms in the rumen help digest otherwise indigestible plant matter, allowing the animal to obtain more nutrients from its food. Unfortunately, a byproduct of this fermentation is methane: a potent greenhouse gas, produced by specific microorganisms in the rumen, burped out by the cattle. Scientists call this “enteric methane,” referring to digestion. The feed, waste, and burping of the vast mass of ruminant livestock accounts for about 14% of global greenhouse gas emissions, with enteric methane accounting for about 4% of global emissions. Unlike a sector like energy production, where technology exists to reduce greenhouse gas emissions, enteric methane emissions has been a point of pessimism: in my view, people will always eat beef, and it is not like you can swap out a rumen with a new stomach part that doesn’t make methane. Reducing emissions from feed and waste – important parts of livestock’s life cycle emissions – is indeed feasible, and in feedlots, where cattle spend a portion of their lives, enteric methane can be physically captured by placing a mask on cattle. Yet absent a cheap, portable way to stop the microorganisms that make methane, cattle will continue to emit massive amounts of methane for the foreseeable future.

But now we do have technology for enteric methane mitigation. As headlines like “Pellet That Stops Cows From Burping Climate-Warming Methane” (Bloomberg, November 29, 2022) allude to, these are drugs that act as antibiotics against the microorganisms that produce methane. The most effective technology reduces cattle methane emissions by 50-90%, with room for improvement. There’s a catch: the technology is the use of halomethanes like bromoform to inhibit methane-producing microorganisms. Halomethanes degrade the ozone layer.

Here I lend a primer, with my views, on the complications of using halomethanes to stop methane emissions from the rumen. These compounds appear to be an effective, cheap, and scalable solution that businesses can develop and profit from. To those of us hoping for another winning solution against climate change, these compounds cannot go to market fast enough, and commercial hurdles for these companies ought to be cleared. However, halomethanes come with concerns, the most serious of which, the potential for degrading the ozone layer, has major repercussions that scientists ought to address, perhaps before the technology is deployed. Finally, as a microbiologist in this scientific area, I feel like we have failed to provide adequate alternatives to address methane mitigation, and I end with a call to action for microbiologists to work on this important problem.

Halomethanes as a way to stop methane production

The microorganisms that produce methane are called methanogens. Like many microorganisms, they have a metabolism that looks nothing like our metabolism. We turn carbon (food) into energy by respiring oxygen, releasing water and carbon dioxide as byproducts. Methanogens obtain energy by converting carbon dioxide, hydrogen, and other compounds into methane. There are different types of methanogens, but all methanogens are single-celled microorganisms in the domain of life called Archaea, which diverged from the domain Bacteria early in Earth’s history. Life as a methanogen is hard: not only are they are sensitive to oxygen, but their metabolism provides very little energy. In order to survive, they need to churn out large amounts of methane. Microbial habitats with little oxygen and lots of organic matter, like the cattle rumen, lead to a lot of methane, perhaps as much as 10% of the carbon fed to the cattle.

Halomethanes affect methanogens because they look like methane. A molecule of methane is a carbon atom surrounded by 4 hydrogen atoms. Unlike methane, halomethanes have one or more hydrogen atoms replaced by an atom of a halogen element such as chlorine or bromine. As early as 1968, microbiologists recognized that the chemical similarity of methane and halomethanes meant that halomethanes would interfere with the enzymes responsible for producing methane, like how a wrench fitting between gears can stop their turning (Wood et. al 1968). Halomethanes interfere with the cellular machinery that makes methane.

The primary issue with halomethanes is that they are gases that can carry halogen atoms aloft. As NOAA explains, above the lower atmosphere, in the stratosphere, is a layer of ozone that protects us by limiting how much ultraviolet radiation reaches Earth’s surface. Halogen-containing gases that persist long enough in the atmosphere can reach the stratosphere. Once in the stratosphere, gases containing halogens can be broken apart, releasing atoms of chlorine or bromine that catalyze the destruction of ozone. With less ozone to absorb ultraviolet light, more UV penetrates the stratosphere and reaches us. The dangers of higher UV exposure led all countries in 1987 to agree to Montreal Protocol phasing out the production of chemicals that destroy the ozone layer, including many halomethanes and all chlorofluorocarbons. (The Montreal Protocol was updated in 2016 to phase out certain halomethanes that are potent greenhouse gases but not ozone-depleting). The Montreal Protocol does not regulate very-short lived gases though recent research indicates these compounds do pose a risk.

A secondary issue with halomethanes, that I do not discuss beyond here, is that they not inert pharmaceuticals that only bind a specific drug target. Halomethanes can act as solvents or as donors of halogen elements to other molecules, resulting in toxicity. For example, chloroform (CHCl₃) at high concentrations can affect liver function and cause mutations leading to cancer (US EPA factsheet). Toxicology is a consideration for any drug, and dose determines determines the effect. So far, trials have demonstrated inhibition of methane inhibition at apparently safe doses. Perhaps there may always be concerns about health risks, even in animals with a short lifetime, among livestock growers (e.g. “Hold off — for now — on feeding seaweed to cows to reduce methane.”) Yet this will be true for any drug given to livestock. The other inhibitor of enteric methane in use, 3-nitropropanol, is also toxic at high enough doses and could have optics issues.

A slow path to seaweed as a source of halomethanes

The Montreal Protocol also eliminated the most obvious solution to cattle emissions. Initial research in the 1990s and 2000s show promising results for bromochloromethane (CH₂ClBr, or “BCM”), commonly used by microbiologists to specifically inhibit methanogens, to stop methane production in the rumen. However, the Montreal Protocol scheduled a stop to bromochloromethane production in 2002. A paper published in 2009 reads as a “swan song” for bromochloromethane:

The experiments reported here were completed in 2004 before the Australian Government prohibited the manufacture and use of [bromochloromethane]. It is unlikely that the [bromochloromethane] formulation will be available for commercial use to mitigate livestock methane emissions in Australia. Nevertheless, the study has demonstrated that methane emissions were substantially reduced over a 90-day feedlot finishing period. This indicates that alternative antimethanogens with a similar mechanism of action may have practical commercial relevance.

Tomkins, N. W., Colegate, S. M., & Hunter, R. A. (2009). A bromochloromethane formulation reduces enteric methanogenesis in cattle fed grain-based diets. Animal Production Science, 49(12), 1053-1058.

With few alternatives identified by microbiologists, animal researchers began to test diverse feedstocks or feed ratios hoping for something to work. The scientific term for this is “throwing things at the wall and seeing what sticks” (humor). Compounds ranged from known inhibitors of methanogen production like fatty acids to various feed additives like cinnamon, garlic, seaweed, and oregano. Where this research stood in 2014 is summarized in this report sponsored by the UN Food Agriculture Organization. One of the successes based on microbiology research, 3-nitropropanol, shows reductions of methane of about 30% and is commercialized by DSM under product name Bovaer. Yet the substance that showed the most reductions in methane was a specific dried red macroalgae Asparagopsis taxiformis, or its cold-water cousin Asaragopsis armata. (Marine macroalgae = seaweed). As scientists like Ermias Kebreab at U.C. Davis have shown to widespread media attention, Asparagopsis can reduce methane emissions over 80%.

You might expect the classic story: after testing substances for bioactivity, scientists find a promising substance and isolate and synthesize the active ingredient. However, the active ingredients in Asaragopsis are… halomethanes. Specifically, Asaragopsis has high amounts of bromoform (CHBr₃) and dibromochloromethane (CHClBr₂). A number of publications stated that these compounds were prohibited under the Montreal Protocol. For example, here is the key paper establishing the active ingredients in Asparagopsis:

Despite the demonstrated efficacy at low concentrations, the use of artificially formulated HMAs [(halogenated methane analogues)] in livestock production systems is prohibited because of their ozone depleting effect. Naturally derived sources of HMAs may provide a practical alternative method for delivery into the rumen. The red macroalga (or seaweed) Asparagopsis taxiformis produces high concentrations of [bromoform] as a secondary metabolite, which accumulates within vacuoles of gland cells.

Machado, L., Magnusson, M., Paul, N. A., Kinley, R., de Nys, R., & Tomkins, N. (2016). Identification of bioactives from the red seaweed Asparagopsis taxiformis that promote antimethanogenic activity in vitro. Journal of Applied Phycology, 28, 3117-3126.

Perhaps out of concern these compounds were prohibited, a number of startups, like Symbrosia and Blue Ocean Barns, began selling Asaragopsis seaweed instead of synthetic bromoform/dibromochloromethane. These companies have had impressive breakthroughs in cultivating algae through aquaculture, instead of harvesting wild seaweed, and in breeding seaweed with improved properties. Blue Ocean Barns is currently testing their product with two upscale California dairies, Straus and Clover. Both companies have done great work that deserves praise. Yet, while cheaper than harvested seaweed, aquaculture-grown seaweed is still expensive. (Plus the U.S.-based companies, both currently in Hawai’i, will be subject to extra shipping costs due to the Jones Act). Symbrosia estimated a cost of $0.80-1.50/day per cattle for their product, perhaps cheaper later, and presumably Blue Ocean Barns would be similar. The product from Blue Oceans Barns is paid for by carbon offsets market to prevent emissions, a relatively great use of offsets that we might expect adopted by other seaweed producers. However, at that cost, can offsets scale to continuous use in hundreds of million of cattle?

This begs the question: are bromoform/dibromochloromethane really prohibited by the Montreal Protocol?

The promise of synthetic halomethanes

Ozone depletion is caused by human-related emissions of ODSs [ozone-depleting substrances] and the subsequent release of reactive halogen gases, especially chlorine and bromine, in the stratosphere . . . The substances controlled under the Montreal Protocol are . . . long-lived (e.g., CFC-12 has a lifetime greater than 100 years) and are also powerful greenhouse gases (GHGs) . . . In addition to the longer-lived ODSs, there is a broad class of chlorine- and bromine-containing substances known as very short-lived substances (VSLSs) that are not controlled under the Montreal Protocol and have lifetimes shorter than about 6 months. For example, bromoform (CHBr₃) has a lifetime of 24 days, while chloroform (CHCl₃) has a lifetime of 149 days. These substances are generally destroyed in the lower atmosphere in chemical reactions. In general, only small fractions of VSLS emissions reach the stratosphere where they contribute to chlorine and bromine levels and lead to increased ozone depletion

UN World Meteorological Organization, Scientific Assessment of Ozone Depletion: 2018, Global Ozone Research and Monitoring Project – Report No. 58, 588 pp., Geneva, Switzerland, 2018.

If the only point of using seaweed was to circumvent the Montreal Protocol, then using seaweed has no point. The UN World Meteorological Organization, the authority on this matter, states that as very-short lived gases, the active ingredients in Asparagopsis are not regulated by the Montreal Protocol. Perhaps they should be, but they are not. Even if they were regulated, these compounds are chemically no different synthesized by algae or synthesized in a factory. If using seaweed to synthesize prohibited halomethanes was a loophole in the Montreal Protocol, we might want to close it.

Halomethanes are very cheap to synthesize using existing chemistry, like the haloform reaction, and halogens extracted from seawater and brines with existing technology (e.g. Octel Bromine Works). Huge amounts of bromine are extracted from brines (and, previously, seawater) from the United States and Israel for synthesizing molecules containing bromine. Bromoform can be purchased in bulk at $0.01 per g (lowest observed quote on vendor websites). An effective dose of Asaragopsis delivers 0.39 g bromoform per day to cattle, meaning the equivalent amount of bromoform would be <$0.01/day per cattle compared to the cost of Asparagopsis at roughly $0.80/day per cattle. Added costs will come from delivering the compound to livestock, which as a gas is trickier than adding powdered seaweed to feed. But gases can be in encapsulated feed, like carbon dioxide in pop-rocks candy, or provided in a slow-release “bolus” object shoved into the rumen, which allows grazing animals outside of feedlots to be dosed.

Synthetic halomethanes are a low-cost solution that can scale as a business. In some instances, methane inhibition has led to faster cattle growth because less carbon is lost to the atmosphere. If the product can be cheap enough to pay for their benefits to cattle growth, cattle growers will pay for it. If not, it’s still a solution that stretches offset funding further, and public policy can aid adoption. Either way, the lower cost advantage is an obvious business opportunity, with an addressable market of hundreds of million of cattle. A new company, Rumin8, uses a feed containing synthetic bromoform, recently received investment from Breakthrough Energy Ventures, and is “on a mission to decarbonise 100 million cattle by 2030.” A new company’s interest is to secure an advantage over likely competitors by building barriers to entry (patents, client relationships, lower unit costs, etc.). Our interest, as a public that wants to limit climate change, is to have several companies providing inhibitors of methane so that prices remain low and more of the market is reached. Based on existing patents and the potential for different delivery options and co-formulations, my opinion is that there is room for a smart company to enter the market successfully.

An argument for Asaragopsis over synthetic halomethanes is that the seaweed currently shows higher efficacy in reducing methane than pure bromoform, perhaps because of different rate of release or the presence of other halomethanes buttressing bromoform. There’s no reason why synthetic halomethanes formulations cannot be optimized to have the same or even greater efficacy than seaweed. With synthetic product instead of an algal product, rate of release can be more easily controlled. Plus, companies could choose from a wide list of very-short lived halomethanes, most of which should be expected to inhibit methanogens, to maximize efficacy while minimizing downsides (cost, health risks, ozone depletion potential, global warming potential, etc.). Companies would be advised, at a minimum, to consider using both bromoform and dibromochloromethane to mimic Asparagopsis. (Very-short lived halomethane gases not regulated by the Montreal Protocol include at least the following: dichloromethane (CH₂Cl₂), chloroform (trichloromethane, CHCl₃), tetrachloroethene (CCl₂CCl₂), trichloroethene (C₂HCl₃) and 1,2-dichloroethane (CH₂ClCH₂Cl), bromoform (CHBr₃), dibromomethane (CH₂Br₂), bromochloromethane (CH₂BrCl), dibromochloromethane (CHBr₂Cl), and bromodichloromethane (CHBrCl₂), methyl iodide (CH₃I), iodochloromethane (CH₂ICl), diiodobromomethane (CH₂IBr), diiodomethane (CH₂I₂) and ethyl iodide (C₂H₅I)).

Seaweed would have taken a long time to scale up production, so perhaps scientists and policymakers expected more time to think. With synthetic halomethanes, the rate limiting step could be simply how quickly the products will be approved and adopted by the market. How many years would it take for large animal feed manufacturer like Cargill from buying a Rumin8-like company for its intellectual property and adding encapsulated bromoform to its products? 2 years? 5 years? Cutting methane emissions has an immediate, important impact on warming. The urgency of the climate crisis means that there will be enormous pressure to scale this technology whether scientists have properly evaluated the risks beforehand or not. Companies, investors, and some growers are certainly are not waiting. It’s time to evaluate synthetic methanes before their widespread use.

The risk of synthetic halomethanes

Reducing methane emissions from enteric fermentation by 50%, e.g. a market penetration of 50% of the global cattle herd of 1 billion at 100% methane mitigation, at 0.39 g bromoform per day requires the synthesis of at least 70 Gg of bromoform per year. Is it worth the risk posed by using so much of an ozone-depleting substance?

Very-short lived gases still contribute to stratospheric ozone depletion. Small amounts do live long enough the stratosphere through mixing, their breakdown products can be longer-living halomethanes like methyl bromide. A more important reason is that atmospheric mixing caused by monsoons gives gases a lift into the stratosphere. In the stratosphere, bromoform is particularly concerning because it carries three bromine atoms, and bromine is a more effective catalyst of ozone degradation than chlorine. The ozone depletion potential of emitted bromoform is estimated to be 1-5 times that of the same mass of CFC-11 (CFCl₃), which is regulated by the Montreal Protocol. Methyl bromide has an ozone depletion potential of 0.57. (Ozone depletion potentials and global warming potentials of halomethanes are defined in Appendix Table A-1 of the Scientific Assessment of Ozone Depletion: 2018). It’s possible bromoform was not regulated simply because it was not synthesized in large quantities. The production of 70 Gg of bromoform per year, estimated above, means the potential emission of 0.07-0.35 Mt/year in CFC-11 equivalents (1 Mt = 1 billion kilograms). That is a very large amount considering annual emissions of ozone depleting gases are currently about 0.3 Mt/year, or double natural emissions. However, if we instead compare to the estimated natural emissions of bromoform at 120-820 Gg/year, synthetic production looks less impactful. (Hence why atmospheric scientists should be performing these analyses).

A key question is: How much of potential emissions will be realized? Halomethanes in the rumen are degraded by methanogens into halide ions like chloride and bromide. No longer in gas form, the risk posed by the halogen atoms has been eliminated for the moment. Companies have touted the degradation of bromoform and other halomethanes as a reason to be reassured about their use. Unfortunately, the science has some holes. We need to know more about the life cycle of halomethanes:

1. How much halomethane gas is released during production and distribution? Companies have some incentive to reduce loss of active ingredient from the product during distribution, as it reduces the quality of the product. However, as we learned with methane extraction from shale (“fracking”), without regulation, companies have no reason to prevent losses during production and manufacturing.
2. How much halomethane gas is lost from the livestock? Methane emissions from the rumen are measured but halomethane emissions are not. Intermediates of halomethane degradation must be measured. Methanogens removed halogen atoms one at a time: for bromoform, from three bromine atoms (bromoform) to two (dibromomethane) to one (methyl bromide) to zero (methane). Because molecules with more halogen atoms are more reactive, they will be degraded first while the intermediate products of the pathway accumulate. This has been shown for chloroform (Krone et. al 1989) and the same should be expected for bromoform and other halomethanes. Also of concern is how often bromoform is not degraded because no methanogens are left to degrade them. Scientists should better quantify how much halomethane is lost in eructed gases.
3. How much halomethane gas is made from livestock waste? In the ideal scenario that all halomethane molecules are converted to halides (e.g. bromide), the salts are excreted from the cow in urine and feces and end up in soil. The story does not end there. Halides are active in soils and can react with organic matter or be taken up by organisms. Bromide is particularly reactive and far less naturally abundant than chlorine. Most importantly, plants can convert bromide to methyl bromide, an ozone-depleting gas. The bromide in soils near the coast, where tides and winds lay sea salt, is one of the natural sources of methyl bromide emissions. In one study, plants immediately take up 95% of bromide added to soil and began to convert some to methyl bromide (Gan et. al 1998). If all bromide in soil ultimately makes it into the atmosphere, perhaps over many years, the use of bromoform in cattle will lead to methyl bromide emissions from soil. Understanding how much and how quickly this occurs is now a critical question.
4. How much will halomethane dose need to be increased? Dose might need to be increased for two reasons. First, as with other antibiotics, methanogens might evolve greater tolerance to halomethanes. Second, halomethanes might be degraded more quickly. Because some microorganisms benefit by breaking down halomethanes, these microorganisms might proliferate in rumens once halomethanes are more widely applied.
5. What is the strength of the ozone-depleting effect and the greenhouse gas effect for a halomethane gas? Choice of which halomethane matters. Gases vary in their ability to contribute to ozone depletion and global warming potential. Halomethanes other than bromoform will have different risk. Bromoform has a negligible global warming potential. Values for dibromochloromethane have not been determined, but bromochloromethane has a global warming potential 17 times that of carbon dioxide and about a fifth that of methane. There is also a geographic dimension to this question: extra precaution should be given to using ozone-depleting substrances in regions with higher risk of transport to the stratosphere, like southeast Asia.

In reality, because of the degradation of bromoform in the rumen, emissions of bromoform will likely be a very small fraction of the potential 0.07-0.35 Mt/year in CFC-11 equivalents. Until the above questions are answered, it would be precautionary to assume that a majority of bromine in bromoform delivered to cattle will ultimately be emitted. It’s also precautionary to limit global warming. Scientists should act now to (1) constrain the above questions to better understand emissions, (2) compare the benefits of enteric methane mitigation to the cost of ozone depletion, and (3) decide acceptable emission thresholds for enteric methane mitigation.

A useful role for public action

Let’s assume that there is some drug for enteric methane inhibition that we want governments to support, not prohibit. How should we do that? I am not an expert in advocacy or policy, but I want to raise the point that the infrastructure is not in place to mobilize this solution.

Compounds that inhibit methanogen production in livestock should have the opportunity to be given emergency regulatory approval. The emergency is the climate crisis. In the United States, at least, regulatory approval by the FDA is too onerous. Livestock growers must be confident that products are safe for use, but the process is too slow for the climate crisis we face. As of 2023, the product Bovaer, which leads to roughly 30% decline in methane emissions, is 6 years into the FDA process for approval as a drug for livestock, but it passed safety and compliance elsewhere and is in use in Europe and countries like Brazil. To avoid the same fate, Rumin8 and the producers of Asparagopsis seem to be trying very hard to be seen as “feed additives” instead of “drugs.” The FDA needs to continue to be lobbied to make the needed process changes, also requested by some in Congress, to expedite bringing drugs for enteric methane inhibition to market. This should have been done years to ago to create incentives for companies to develop solutions.

A more important barrier to adoption is that livestock growers currently have little incentive to use products that inhibit enteric methane production. The economic prerogative is for growers to sell tasty meat and milk, not to reduce methane emissions. Many growers will be personally and culturally averse the notion that their livestock are causing environmental harm. Enteric methane inhibitors could provide a growth advantage, which would lead slowly to adoption. But let’s assume they provide no benefit or an ambiguous benefit. Why take on an extra cost, not borne by your competitors, with no benefit? Do not delude yourself into thinking growers opting in will make even a dent in this problem.

A subset of customers who are environmentally conscious will pay a premium for products certified to produce lower methane emissions. I imagine many consumers would pay a hefty premium for certified “Low Methane” / “Minimal Methane” beef, milk, and cheese. The ability to obtain a premium from customers will create an economic incentive for many growers, though not all growers, to use a cost-effective methane inhibitor. Currently, there is no certifying organization. Should there be one, it ought to have a mission to provide an economic benefit to growers with truly low methane methods. An environmental organization with trust among growers should step into the void before organizations with other goals step in. For example, the American Feed Industry Association (AFIA) has been an advocate of this technology but make specious claims like “with just a 20-30 percent reduction in methane emissions, the entire livestock industry can be climate neutral in the next two decades.” We need a certifying organization to require close >90% reduction in enteric methane emissions, ideally plus emissions reduction through manure management, while also receiving backing from growers.

How long should we rely on consumer preference? After all, U.S. beef consumption per capita has increased in recent years. Governments should eventually create new regulations to ensure that the livestock industry adopts methane limiting practices. Forcing a cost on everyone is a relatively fair way because no grower has taken up the extra cost; however, it may place greater economic burden on smaller operations that do not have the benefit of scale, and no one likes new taxes (see: “New Zealand angers its farmers by proposing taxing cow burps“). Another route is to use subsidies. Governments heavily subsidize the production of livestock because people want cheap meat. Governments could create an additional subsidy that is conditional on the effective use of methane inhibiting products – a giveaway to an industry, but an investment in our future. Crucially, government mandated used of a product that has environmental or health concerns will lead to more pushback. Products should be trusted prior to this step.

Finally, how can we reach cattle growers in different types of farming operations? Obviously, we know where to start. For example, in the United States, the USDA reports that “although feedlots with 1,000-head-or-greater capacity are less than 5 percent of total feedlots, they market 80–85 percent of fed cattle. Feedlots with a capacity of 32,000 head or more market around 40 percent of fed cattle.” Starting commercially with the large, concentrated, industrialized operations in wealthy countries provides greater impact and business opportunity. In other countries, the costs may outweigh benefits, and there may be a role for governments to subsidize use by countries with less purchasing power, like for some other drugs.

A need for leadership from microbiologists

For a problem of its magnitude, too little effort has gone into finding inhibitors of methane emissions from cattle. I found only two papers in the last decade that screen for new inhibitors of methane, and one was a computational screen whose purpose was to stop irritable bowel syndrome (to be fair, that is definitely the world’s #2 concern behind global warming). Microbiologists have not even determined which halomethane would be the best inhibitor, alone or in combination, yet here we are going to market with pure bromoform.

(An aside: I am embarrassed that, in the 2010s, when the need for microbiology research on climate solutions was so obvious, I did my Ph.D. research on a topic in microbial metabolism that did nothing to address climate change. I, like many other scientists, worked on something that was best for my career, or that fit into the laboratory/grants I joined, or that I convinced myself was useful just because it was science. I figured someone else was working on this question.)

I want to speak directly to microbiologists. We need more options, ASAP. Studying methanogen biology is not enough. To have the most impact you could ever have studying methanogens, you do not need to know any more about methanogen physiology or about methanogen genomes or about the rumen microbiome or about rumens. You just need to find more molecules that kill methanogens. You could even take a shortcut and kill archaea, which includes all methanogens, so long as the compound isn’t toxic to other rumen microorganisms or the animal host. Identifying new inhibitors of archaea or methanogens can be done several different ways, fitting into various existing research programs that probe archaeal biology.

The criteria for such a screen would look for chemicals with:

• Specificity for methanogens or archaea in general
• Low cost
• Low animal health / environmental concerns
• Stability during production and delivery
• Palatability to livestock
• Ability act in synergy with other inhibitors by targeting different mechanisms (preferred)

Here’s a start. What’s known to inhibit methanogens so far? A handful of reviews summarize how to inhibit methanogens (Liu et. al 2011, Henderson et. al 2016, Czatzkowska et. al 2020), which are of a few different types. One type of inhibitors, like volatile fatty acids and electron acceptors (e.g. nitrate), act by affecting the methanogen’s habitat and are therefore less useful in the rumen. Bromoform, bromochloromethane (BCM), and Bovaer (3-nitropropanol) are among a type, with other reactive compounds like acetelyne and ethylene, that react with a key enzyme in methanogens. Another type of inhibitors, like 2-bromoethanesulfonate (BES) and lumazin, resemble a molecule in enzymes found only in methanogens. A final class of inhibitors are those that inhibit archaea generally, which to my knowledge only currently includes statins. Statins should sound familiar for their use in inhibiting cholesterol biosynthesis in humans. Archaea use the same biosynthesis pathway but for a more essential purpose: they use compounds from that pathway to build their cellular membrane. Statins are promising enteric methane inhibitors but too costly to synthesize (allegedly). Finally, there are inhibitors with no know mechanism, like those identified in a screen by Weimar et. al 2017 testing a commercial library of 1200 compounds, with a few leads.

That’s it. Everything you know as a microbiologist to be a specific inhibitor of methanogens has only gotten us this far in enteric methane mitigation, and to my knowledge no one is looking for new inhibitors. I am optimistic that, because archaea and methanogens have been understudied, there are inhibitors that can be discovered through reasonable effort. I am also optimistic that someone will test for cost-effective combinations or variations among existing effective chemicals like halomethanes, nitroxy groups (e.g. 3-nitropropanol), and statins. I am even cautiously optimistic that some microbiologists will step up the occasion and recognize their duty to act.

[Edit: since posting I’ve learned about ongoing proprietary research by the New Zealand Pastoral Greenhouse Gas Research Consortium (PGgRc), continuing work from Weimar et. al]

Conclusion

To answer the question in the title: we don’t know if we are moving too fast or too slow because we haven’t reached scientific consensus on the trade-off. We need enteric methane inhibitors to reduce the portion of greenhouse gas emissions that come from livestock’s stomachs. The inhibitors we have, bromoform and 3-nitropropanol, are imperfect in their own ways. The most effective inhibitor, bromoform, is so cheap to make in huge quantities that use in 100 million cattle by 2030 is, to me, not unreasonable. Concerns about its effect on ozone need to be resolved now and, in the absence of other effective enteric methane inhibitors, weighed against the cost of the methane emissions from doing nothing. Interested parties – from atmospheric scientists and microbiologists to climate advocacy groups – should recognize the opportunity for a huge step forward and the risk of taking a misstep. Right now most of us have been caught flat-footed.