Subclinical ketosis as a driver of enteric greenhouse gas emissions in dairy cows

Dairy cattle are a major contributor to greenhouse gas (GHG) emissions, primarily through enteric methane (CH₄) production [1]. While mitigation strategies have traditionally focused on diet formulation and genetics, the influence of metabolic disorders on enteric gas emissions has received limited attention [2,3]. Subclinical ketosis (SCK), a metabolic disease of early lactation, affects energy metabolism, feed efficiency, and rumen fermentation[4]. The aim of this study was to quantify the effects of SCK on enteric CH₄, carbon dioxide (CO₂), and hydrogen (H₂) emissions, as well as on production efficiency, in early-lactation dairy cows. A total of 60 multiparous Holstein–Friesian cows were enrolled in a longitudinal study from 3 to 28 days in milk (DIM). Individual daily emissions of CH₄, CO₂, and H₂ were measured using an automated GreenFeed system. Blood β-hydroxybutyrate (BHB) concentrations were measured at 7, 14, 21, and 28 DIM to divide cows as healthy controls (CTR; BHB < 1.0 mmol/L at all time points; n = 43) or affected by SCK (KET; BHB ≥ 1.0 mmol/L at least once; n = 17). Statistical analysis was conducted with linear mixed models and p≤0.05 was used as significant. Cows affected by SCK produced significantly more CH₄ than healthy cows, with average emissions of 402.8 ± 26.6 g/day in KET cows compared with 243.8 ± 17.7 g/day in CTR cows, corresponding to a 65% increase. When expressed as CO₂ equivalents (GWP₁₀₀ = 27.2), CH₄ emissions amounted to 10.96 ± 0.72 kg CO₂e/day in KET cows vs 6.60 ± 0.48 kg CO₂e/day in CTR cows. The CH₄ intensity was markedly higher in KET cows, both per kilogram of milk (12.8 ± 1.2 vs. 7.7 ± 0.8 g CH₄/kg milk) and per kilogram of dry matter intake, indicating reduced metabolic and productive efficiency. In contrast, direct CO₂ emissions were lower in KET cows (11,035 ± 593 vs. 12,225 ± 416 g/day), and H₂ emissions were also reduced, suggesting enhanced H₂ utilization by methanogenic archaea. The analysis around the onset of SCK revealed a rapid increase in CH₄ emissions immediately after diagnosis, persisting for several days. Despite lower CO₂ output, the higher CH₄-derived CO₂ equivalents resulted in a greater overall GHG footprint in cows affected by SCK. These results demonstrate that metabolic health is a key driver of enteric GHG emissions and highlight the potential of SCK prevention as a complementary strategy to improve both production efficiency and environmental sustainability in dairy systems. [1] U.S. EPA Global Non-CO2 Greenhouse Gas Emission Projections & Mitigation Potential: 2015-2050 | US EPA; 2019. [2] Danielsson, R.; Dicksved, J.; Sun, L.; Gonda, H.; Müller, B.; Schnürer, A.; Bertilsson, J. Methane Production in Dairy Cows Correlates with Rumen Methanogenic and Bacterial Community Structure. Front. Microbiol. 2017, 8, doi:10.3389/FMICB.2017.00226. [3] Pitta, D.; Indugu, N.; Narayan, K.; Hennessy, M. Symposium Review: Understanding the Role of the Rumen Microbiome in Enteric Methane Mitigation and Productivity in Dairy Cows. J. Dairy Sci. 2022, 105, 8569–8585, doi:10.3168/JDS.2021-21466. [4] Zhang, G.; Ametaj, B.N. Ketosis an Old Story Under a New Approach. Dairy 2020, Vol. 1, Pages 42-60 2020, 1, 42–60, doi:10.3390/DAIRY1010005.