Isoprene (2-methyl-1,3-butadiene) is a significant biogenic volatile organic compound (BVOC) with emissions comparable to methane. Its atmospheric reactivity leads to ozone formation, influencing the oxidation of other compounds and contributing to secondary organic aerosols. While terrestrial sources (trees, shrubs) are well-studied, marine isoprene emissions remain uncertain, with top-down (atmospheric observations) and bottom-up (oceanic concentration and flux modeling) estimates differing by orders of magnitude (0.1–12 TgC year⁻¹). This discrepancy highlights a lack of understanding of oceanic isoprene cycling processes, particularly the magnitude and drivers of isoprene degradation in seawater. This study addresses this knowledge gap by investigating the chemical and biological consumption of isoprene in the surface ocean, aiming to provide better constraints on global marine isoprene emissions and improve atmospheric models.

Previous research has established that phytoplankton and seaweeds are primary marine isoprene producers. The ecological role of isoprene biosynthesis in phytoplankton is unclear, though an antioxidant function has been hypothesized. While chemical oxidation is assumed due to isoprene's high reactivity, it has not been directly measured in the ocean. Similarly, the existence of isoprene-degrading bacteria has been demonstrated, but its significance in natural conditions and at natural concentrations remains unquantified. Existing models of the global oceanic isoprene cycle employ either fixed or variable microbial consumption rates, but these are largely based on assumptions and limited data. A previous study suggested a significant photochemical isoprene source through surfactants in the sea surface microlayer, but its contribution to resolving the discrepancy in emission estimates remains debated. Thus, a lack of comprehensive measurements of isoprene loss processes hinders accurate assessment of the marine isoprene cycle.

The study employed seawater incubation experiments to quantify isoprene consumption. Coastal seawater incubations in closed glass bottles, under dark conditions to arrest production, revealed sustained isoprene loss over 45 hours. By comparing isoprene loss in filtered and unfiltered water, the researchers separated chemical oxidation from microbial degradation. The addition of hydrogen peroxide (H₂O₂) and bromoperoxidase (BrPO) significantly accelerated isoprene loss, suggesting H₂O₂-mediated chemical oxidation either directly or via HOBr (produced enzymatically by BrPO). Eleven offshore experiments, conducted across diverse oceanic regions (Mediterranean, Atlantic, tropical Pacific, Antarctic, Subantarctic), involved 24-hour dark incubations of unfiltered surface seawater. First-order loss rate constants (kloss) were determined from initial and final isoprene concentrations, assuming dark conditions arrested production (though acknowledging potential for residual production). These kloss values were compared with air-sea flux (kvent) and vertical mixing (kmix) rate constants. The relationship between kloss and environmental/biological variables (chlorophyll-a concentration, bacterial abundance, temperature) was analyzed to develop a predictive model for isoprene loss. Isoprene concentration was measured using gas chromatography-mass spectrometry (GC-MS). Ventilation rates (kvent) were estimated using a gas exchange velocity model incorporating wind speed and Schmidt number. Vertical mixing rates (kmix) were estimated from vertical isoprene concentration profiles (where available) and turbulent diffusion coefficients. Chlorophyll-a concentration was measured using fluorometry, and bacterial abundance using flow cytometry. A steady-state assumption (A[iso]/At = 0) over 24 hours was used to estimate isoprene production rates (kprod).

Coastal seawater incubations demonstrated a combined chemical and biological isoprene loss, with chemical oxidation accounting for approximately half of the total loss. Offshore experiments showed kloss varied considerably (0.03–0.64 d⁻¹, median 0.08 d⁻¹), exhibiting a strong positive correlation with chlorophyll-a concentration (R² = 0.96, p = 10⁻⁷). A linear regression model was developed: kloss = 0.10 (±0.01) × [chla] + 0.05 (±0.01). The intercept (0.05 d⁻¹) represents a constant chemical loss rate, consistent with previous model estimations. The chlorophyll-a dependent term (0.10 × [chla]) represents biological consumption, varying between 0 and 0.59 d⁻¹ (median 0.03 d⁻¹). In most sampling sites, isoprene loss via microbial and chemical consumption was of the same order of magnitude or even greater than ventilation to the atmosphere. The total turnover time of isoprene ranged from 1.4 to 16 days, with a median of 5 days. Specific isoprene production rates (chla-normalized) showed exponential increase with temperature up to 23°C, followed by a decrease at higher temperatures, a pattern similar to that observed for Prochlorococcus. This suggests that temperature is a key factor influencing isoprene production rates, beyond simply the biomass of chlorophyll-a. The study notes that the relationship between kloss and chlorophyll-a concentration can be adapted for use with satellite-derived chlorophyll data, providing a method for estimating isoprene loss rates remotely.

The findings significantly advance our understanding of isoprene cycling in the surface ocean. The strong correlation between isoprene loss and chlorophyll-a concentration indicates a crucial role for biological consumption, mainly through microbiota, in regulating oceanic isoprene levels. This contrasts with the previous assumption of ventilation as the dominant sink. The established linear relationship between kloss and chlorophyll-a allows for improved predictions of isoprene loss rates, particularly in productive waters. The observed temperature dependency of isoprene production highlights the importance of considering environmental stressors beyond just phytoplankton biomass. The model developed provides a more accurate representation of isoprene turnover in the ocean, addressing the limitations of previous models that relied on fixed loss rates.

This research provides novel experimental evidence of significant isoprene loss in the surface ocean due to both chemical and biological processes, with the latter strongly linked to chlorophyll-a concentrations. The developed model, incorporating both chemical and chlorophyll-dependent biological loss rates, substantially improves our ability to predict oceanic isoprene cycling. Future studies should focus on identifying the specific microorganisms and metabolic pathways involved in isoprene biological consumption, and investigating the influence of various environmental factors on isoprene biosynthesis in phytoplankton to improve model accuracy. A more comprehensive understanding of these processes will be crucial for improving the accuracy of global climate models.

The study acknowledges that residual isoprene production might have occurred in the dark incubations, potentially underestimating kloss. The number of offshore experiments, while covering diverse oceanic regions, might be limited for robust global generalizations. The conversion of fluorometric to satellite chlorophyll-a concentrations introduces uncertainty due to differences in measurement methods. Furthermore, the exact metabolic pathways and microbial players responsible for isoprene consumption are not identified.