Vaughan T. J. Phillips

Major volcanic eruptions have long been proposed to have triggered and amplified historical plague pandemics through climatic shocks and harvest failures, but the mechanisms linking volcanic forcing, nutrition and disease remain poorly quantified. We develop a theoretical model of a single region with zero spatial dimensions ("0-D") that couples volcanic forcing, climate, agricultural productivity, food storage, malnutrition and plague epidemiology. The epidemiological component includes reservoir hosts, vectors, human-to-human transmission, disease-driven migration and waning immunity, with transmission and mortality rates dependent on nutritional status. We first evaluate the model against agricultural and archaeological evidence from England following the 1345 CE eruption, shortly before the Second Plague Epidemic. The simulations reproduce the observed sudden drop in crop output and prolonged deterioration in nutritional conditions, as well as the observed relationship between plague mortality and an isotopic proxy for malnutrition derived from human skeletons. We then apply the model to the Justinianic Plague following the 536 and 540 CE eruptions. Representing three population groups with different vulnerability to harvest failure and malnutrition, the model predicts eventual plague mortality of about 39 %, consistent with historical estimates. Sensitivity experiments show that removing the effect of volcanic forcing on malnutrition substantially reduces predicted plague mortality, whereas excluding disease-driven migration increases it. Doubling eruption intensity produces only a modest increase in total mortality, revealing nonlinear interactions among climate, nutrition and epidemic dynamics. A reduced phase-space analysis further shows that epidemic feedbacks change from net positive to net negative as susceptible individuals are depleted, with the system transitioning from an initially unstable state towards a quasi-equilibrium attractor. Together, the simulations suggest that volcanic eruptions could have substantially amplified historical plague epidemics through their effects on failure of harvests and food production, malnutrition and human behaviour. The results provide a mechanistic framework linking volcanic climate forcing to epidemic severity and highlight nutrition as a potentially important mediator of climate–disease interactions.

Major volcanic eruptions have long been proposed to have triggered and amplified historical plague pandemics through climatic shocks and harvest failures, but the mechanisms linking volcanic forcing, nutrition and disease remain poorly quantified. We develop a theoretical model of a single region with zero spatial dimensions ("0-D") that couples volcanic forcing, climate, agricultural productivity, food storage, malnutrition and plague epidemiology. The epidemiological component includes reservoir hosts, vectors, human-to-human transmission, disease-driven migration and waning immunity, with transmission and mortality rates dependent on nutritional status. We first evaluate the model against agricultural and archaeological evidence from England following the 1345 CE eruption, shortly before the Second Plague Epidemic. The simulations reproduce the observed sudden drop in crop output and prolonged deterioration in nutritional conditions, as well as the observed relationship between plague mortality and an isotopic proxy for malnutrition derived from human skeletons. We then apply the model to the Justinianic Plague following the 536 and 540 CE eruptions. Representing three population groups with different vulnerability to harvest failure and malnutrition, the model predicts eventual plague mortality of about 39 %, consistent with historical estimates. Sensitivity experiments show that removing the effect of volcanic forcing on malnutrition substantially reduces predicted plague mortality, whereas excluding disease-driven migration increases it. Doubling eruption intensity produces only a modest increase in total mortality, revealing nonlinear interactions among climate, nutrition and epidemic dynamics. A reduced phase-space analysis further shows that epidemic feedbacks change from net positive to net negative as susceptible individuals are depleted, with the system transitioning from an initially unstable state towards a quasi-equilibrium attractor. Together, the simulations suggest that volcanic eruptions could have substantially amplified historical plague epidemics through their effects on failure of harvests and food production, malnutrition and human behaviour. The results provide a mechanistic framework linking volcanic climate forcing to epidemic severity and highlight nutrition as a potentially important mediator of climate–disease interactions.

Major volcanic eruptions have long been proposed to have triggered and amplified historical plague pandemics through climatic shocks and harvest failures, but the mechanisms linking volcanic forcing, nutrition and disease remain poorly quantified. We develop a theoretical model of a single region with zero spatial dimensions ("0-D") that couples volcanic forcing, climate, agricultural productivity, food storage, malnutrition and plague epidemiology. The epidemiological component includes reservoir hosts, vectors, human-to-human transmission, disease-driven migration and waning immunity, with transmission and mortality rates dependent on nutritional status. We first evaluate the model against agricultural and archaeological evidence from England following the 1345 CE eruption, shortly before the Second Plague Epidemic. The simulations reproduce the observed sudden drop in crop output and prolonged deterioration in nutritional conditions, as well as the observed relationship between plague mortality and an isotopic proxy for malnutrition derived from human skeletons. We then apply the model to the Justinianic Plague following the 536 and 540 CE eruptions. Representing three population groups with different vulnerability to harvest failure and malnutrition, the model predicts eventual plague mortality of about 39 %, consistent with historical estimates. Sensitivity experiments show that removing the effect of volcanic forcing on malnutrition substantially reduces predicted plague mortality, whereas excluding disease-driven migration increases it. Doubling eruption intensity produces only a modest increase in total mortality, revealing nonlinear interactions among climate, nutrition and epidemic dynamics. A reduced phase-space analysis further shows that epidemic feedbacks change from net positive to net negative as susceptible individuals are depleted, with the system transitioning from an initially unstable state towards a quasi-equilibrium attractor. Together, the simulations suggest that volcanic eruptions could have substantially amplified historical plague epidemics through their effects on failure of harvests and food production, malnutrition and human behaviour. The results provide a mechanistic framework linking volcanic climate forcing to epidemic severity and highlight nutrition as a potentially important mediator of climate–disease interactions.

Major volcanic eruptions have long been proposed to have triggered and amplified historical plague pandemics through climatic shocks and harvest failures, but the mechanisms linking volcanic forcing, nutrition and disease remain poorly quantified. We develop a theoretical model of a single region with zero spatial dimensions ("0-D") that couples volcanic forcing, climate, agricultural productivity, food storage, malnutrition and plague epidemiology. The epidemiological component includes reservoir hosts, vectors, human-to-human transmission, disease-driven migration and waning immunity, with transmission and mortality rates dependent on nutritional status. We first evaluate the model against agricultural and archaeological evidence from England following the 1345 CE eruption, shortly before the Second Plague Epidemic. The simulations reproduce the observed sudden drop in crop output and prolonged deterioration in nutritional conditions, as well as the observed relationship between plague mortality and an isotopic proxy for malnutrition derived from human skeletons. We then apply the model to the Justinianic Plague following the 536 and 540 CE eruptions. Representing three population groups with different vulnerability to harvest failure and malnutrition, the model predicts eventual plague mortality of about 39 %, consistent with historical estimates. Sensitivity experiments show that removing the effect of volcanic forcing on malnutrition substantially reduces predicted plague mortality, whereas excluding disease-driven migration increases it. Doubling eruption intensity produces only a modest increase in total mortality, revealing nonlinear interactions among climate, nutrition and epidemic dynamics. A reduced phase-space analysis further shows that epidemic feedbacks change from net positive to net negative as susceptible individuals are depleted, with the system transitioning from an initially unstable state towards a quasi-equilibrium attractor. Together, the simulations suggest that volcanic eruptions could have substantially amplified historical plague epidemics through their effects on failure of harvests and food production, malnutrition and human behaviour. The results provide a mechanistic framework linking volcanic climate forcing to epidemic severity and highlight nutrition as a potentially important mediator of climate–disease interactions.

Major volcanic eruptions have long been proposed to have triggered and amplified historical plague pandemics through climatic shocks and harvest failures, but the mechanisms linking volcanic forcing, nutrition and disease remain poorly quantified. We develop a theoretical model of a single region with zero spatial dimensions ("0-D") that couples volcanic forcing, climate, agricultural productivity, food storage, malnutrition and plague epidemiology. The epidemiological component includes reservoir hosts, vectors, human-to-human transmission, disease-driven migration and waning immunity, with transmission and mortality rates dependent on nutritional status. We first evaluate the model against agricultural and archaeological evidence from England following the 1345 CE eruption, shortly before the Second Plague Epidemic. The simulations reproduce the observed sudden drop in crop output and prolonged deterioration in nutritional conditions, as well as the observed relationship between plague mortality and an isotopic proxy for malnutrition derived from human skeletons. We then apply the model to the Justinianic Plague following the 536 and 540 CE eruptions. Representing three population groups with different vulnerability to harvest failure and malnutrition, the model predicts eventual plague mortality of about 39 %, consistent with historical estimates. Sensitivity experiments show that removing the effect of volcanic forcing on malnutrition substantially reduces predicted plague mortality, whereas excluding disease-driven migration increases it. Doubling eruption intensity produces only a modest increase in total mortality, revealing nonlinear interactions among climate, nutrition and epidemic dynamics. A reduced phase-space analysis further shows that epidemic feedbacks change from net positive to net negative as susceptible individuals are depleted, with the system transitioning from an initially unstable state towards a quasi-equilibrium attractor. Together, the simulations suggest that volcanic eruptions could have substantially amplified historical plague epidemics through their effects on failure of harvests and food production, malnutrition and human behaviour. The results provide a mechanistic framework linking volcanic climate forcing to epidemic severity and highlight nutrition as a potentially important mediator of climate–disease interactions.

Major volcanic eruptions have long been proposed to have triggered and amplified historical plague pandemics through climatic shocks and harvest failures, but the mechanisms linking volcanic forcing, nutrition and disease remain poorly quantified. We develop a theoretical model of a single region with zero spatial dimensions ("0-D") that couples volcanic forcing, climate, agricultural productivity, food storage, malnutrition and plague epidemiology. The epidemiological component includes reservoir hosts, vectors, human-to-human transmission, disease-driven migration and waning immunity, with transmission and mortality rates dependent on nutritional status. We first evaluate the model against agricultural and archaeological evidence from England following the 1345 CE eruption, shortly before the Second Plague Epidemic. The simulations reproduce the observed sudden drop in crop output and prolonged deterioration in nutritional conditions, as well as the observed relationship between plague mortality and an isotopic proxy for malnutrition derived from human skeletons. We then apply the model to the Justinianic Plague following the 536 and 540 CE eruptions. Representing three population groups with different vulnerability to harvest failure and malnutrition, the model predicts eventual plague mortality of about 39 %, consistent with historical estimates. Sensitivity experiments show that removing the effect of volcanic forcing on malnutrition substantially reduces predicted plague mortality, whereas excluding disease-driven migration increases it. Doubling eruption intensity produces only a modest increase in total mortality, revealing nonlinear interactions among climate, nutrition and epidemic dynamics. A reduced phase-space analysis further shows that epidemic feedbacks change from net positive to net negative as susceptible individuals are depleted, with the system transitioning from an initially unstable state towards a quasi-equilibrium attractor. Together, the simulations suggest that volcanic eruptions could have substantially amplified historical plague epidemics through their effects on failure of harvests and food production, malnutrition and human behaviour. The results provide a mechanistic framework linking volcanic climate forcing to epidemic severity and highlight nutrition as a potentially important mediator of climate–disease interactions.

Much of the initiation of ice particles in deep precipitating clouds has been attributed to secondary ice production (SIP). Fragmentation during collisions among particles of ice precipitation is one of the known SIP processes. Some recent studies have used our theoretical formulation of this SIP process in the cloud microphysics scheme of numerical atmospheric models published in 2017. However, there has been a lack of observational data for better understanding of SIP processes. The focus of the present study is on fragmentation of naturally falling snowflakes during their collisions with graupel/hail particles, based on observations conducted at Jungfraujoch, a mountain pass in the Alps and located at about 3.6 km above mean sea level. The cloud top was from −25° to −32°C and cloud base at about −16°C. The study used a portable chamber specially designed to observe the fragmentation of snow particles outdoors. The detection threshold for counting fragments was about 0.2 mm. Fixed ice spheres in the chamber were used to mimic graupel or hail. Based on the observational study, we optimized the theoretical formulation for prediction of the number of fragments arising from collisions between snow and graupel/hail. The observations reveal an average number of fragments per collision of about 5. The study improved the prediction of SIP by this type of fragmentation compared to our original theoretical formulation, for snow consisting of mostly aggregates of crystals from the “nondendritic habit regime” of temperatures colder than −17°C. Significance Statement: This work advances knowledge about fragmentation of snow aloft, which is a process dominating the secondary ice production in natural clouds. Better empirical characterization of this process of initiation of cloud–ice particles allows its representation in atmospheric models, improving the quality of simulations.

Major volcanic eruptions have long been proposed to have triggered and amplified historical plague pandemics through climatic shocks and harvest failures, but the mechanisms linking volcanic forcing, nutrition and disease remain poorly quantified. We develop a theoretical model of a single region with zero spatial dimensions ("0-D") that couples volcanic forcing, climate, agricultural productivity, food storage, malnutrition and plague epidemiology. The epidemiological component includes reservoir hosts, vectors, human-to-human transmission, disease-driven migration and waning immunity, with transmission and mortality rates dependent on nutritional status. We first evaluate the model against agricultural and archaeological evidence from England following the 1345 CE eruption, shortly before the Second Plague Epidemic. The simulations reproduce the observed sudden drop in crop output and prolonged deterioration in nutritional conditions, as well as the observed relationship between plague mortality and an isotopic proxy for malnutrition derived from human skeletons. We then apply the model to the Justinianic Plague following the 536 and 540 CE eruptions. Representing three population groups with different vulnerability to harvest failure and malnutrition, the model predicts eventual plague mortality of about 39 %, consistent with historical estimates. Sensitivity experiments show that removing the effect of volcanic forcing on malnutrition substantially reduces predicted plague mortality, whereas excluding disease-driven migration increases it. Doubling eruption intensity produces only a modest increase in total mortality, revealing nonlinear interactions among climate, nutrition and epidemic dynamics. A reduced phase-space analysis further shows that epidemic feedbacks change from net positive to net negative as susceptible individuals are depleted, with the system transitioning from an initially unstable state towards a quasi-equilibrium attractor. Together, the simulations suggest that volcanic eruptions could have substantially amplified historical plague epidemics through their effects on failure of harvests and food production, malnutrition and human behaviour. The results provide a mechanistic framework linking volcanic climate forcing to epidemic severity and highlight nutrition as a potentially important mediator of climate–disease interactions.

Large-scale stratiform clouds are widespread and dominate the Earth's radiation budget. Their radiative and microphysical properties are inseparable, depending on ambient aerosol conditions and on properties of any convective outflow. In the Community Atmospheric Model, version 6 (CAM6), large-scale clouds were originally treated two decades ago with a two-moment bulk microphysics approach. Since then, the technological and empirical basis of global models has improved, for example by representing cloud microphysics to encompass extra processes of ice and droplet initiation, and by including dependencies on aerosol conditions of size, composition, and loading. To advance the microphysical realism of the large-scale cloud scheme of the global model CAM6, most of the known mechanisms of secondary ice production (SIP) and an empirical formulation for heterogeneous ice nucleation have been represented in the stratiform scheme of the Global model CAM6. We included a hybrid bin/bulk microphysics scheme that treats aerosol activation, growth processes of accretion, aggregation, and riming, and three SIP mechanisms in the stratiform cloud scheme. We simulated an observed case of a mesoscale convective system during the Mid-latitude Continental Convective Clouds Experiment (MC3E) in Oklahoma, USA, using the Single-Column Atmosphere Model (SCAM6). The results from the simulations are validated against the aircraft, satellite, and ground measurements. Results show that the modified stratiform scheme can predict the cloud properties of the observed stratiform clouds realistically. Together with our improved convective scheme in CAM6, this paves the way for more realism in the treatment of aerosol-cloud interactions in global climate change by conventional General Circulation Models.

Secondary ice production explains why clouds often contain ice particle concentrations that are orders of magnitude higher than the number of ice-nucleating particles available to initiate freezing. Accurate prediction of concentrations of ice in atmospheric clouds necessitates an understanding of SIP mechanisms. A fundamental challenge is determining how modeled SIP mechanisms depend on cloud properties and environmental conditions.In this study, we used the Aerosol–Cloud (AC) model, which incorporates four secondary ice production mechanisms: ice–ice collisional breakup, fragmentation during raindrop freezing, the Hallett–Mossop process, and sublimational breakup. The various numerical simulations for sensitivity studies are conducted with the AC model and evaluated using a control simulation. Ice multiplication is driven by positive feedback mechanisms formed by interconnected microphysical processes. Investigating the potential for ice enhancement in natural clouds therefore requires consideration of the full range of microphysical interactions that may either suppress or amplify its influence under varying environmental conditions. The objective is to assess and determine the synergy among the secondary ice mechanisms.In tropical deep convective clouds with very warm cloud bases, lower environmental CCN concentrations led to higher simulated ice concentrations in the lower mixed-phase region. In contrast, plausible variations in environmental IN concentrations had little effect on total simulated ice at any altitude. Overall, ice multiplication acted to dampen the simulated sensitivity to changes in both IN and CCN aerosol loadings.