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Climate change and public health is an interdisciplinary field that draws on Earth system science, epidemiology, human physiology, and public health to understand how changes in the global climate alter patterns of human illness, death, and physiological stress. Climate change rarely introduces entirely new diseases. Instead, it acts as a risk multiplier, altering the physical and ecological conditions that shape health: heat exposure, air quality, water supply, the ecology of pathogens, and food security.

Climate-related health effects are commonly grouped into three pathways:

1. Direct exposures: injury, illness, and death caused by changes in the frequency, duration, and intensity of extreme events such as heat waves, flash floods, tropical cyclones, and wildfires.
2. Ecologically mediated pathways: changes in the range, reproduction, and transmission efficiency of arthropod vectors, animal reservoirs of disease, waterborne bacteria, and harmful algal blooms, as well as changes in air pollution and airborne allergens.
3. Socially and economically mediated pathways: disruption of crop yields, fisheries, and the nutritional content of staple foods, leading to undernutrition, micronutrient deficiencies, lost work capacity, and displacement of populations.

Vector-borne diseases are caused by viruses, bacteria, protozoa, or helminths transmitted between vertebrate hosts by blood-feeding arthropods, principally mosquitoes (Culicidae), ticks (Ixodida), sandflies (Phlebotominae), and blackflies (Simuliidae). Arthropods are ectotherms: their body temperature follows that of their surroundings. As a result, their development, survival, and biting behaviour, and the replication of the pathogens they carry, all depend strongly on temperature.

The link between climate and vector-borne transmission is formalized by the Ross–Macdonald model, developed by Ronald Ross and George Macdonald. Whether an infection can spread in a population is determined by the basic reproduction number R₀, the expected number of secondary infections caused by one infected person in a fully susceptible population:

where b and c are the probabilities of transmission from vector to human and from human to vector, and r is the human recovery rate. The entomological part of this expression is the vectorial capacity V, the number of potentially infective bites arising each day from a single infectious person:

so that R₀ = V b c / r. Each entomological parameter depends on temperature (T), and several also depend on rainfall and humidity:

• m is the number of female vectors per person. It depends on the availability of larval habitat, set by the balance between rainfall and evaporation, and on temperature-dependent development rates.
• a is the daily rate at which a vector bites humans. It is related to the length of the gonotrophic cycle, the time needed to digest a blood meal and produce eggs. a appears squared because a vector must bite once to acquire the pathogen and again to transmit it, so faster digestion at higher temperatures has a disproportionately large effect.
• p = e^−_μ_ is the daily survival probability of adult vectors, where μ is the daily mortality rate and 1/_μ_ is the mean adult lifespan.
• n is the extrinsic incubation period (EIP), the number of days after an infectious blood meal before the pathogen reaches the vector's salivary glands and can be transmitted.

Because the extrinsic incubation period appears in an exponent, the proportion of vectors that survive long enough to become infectious (pⁿ = e^−_μn_) is very sensitive to changes in n. In the classical degree-day model, _n_(T) = DD/(T − T_min), where DD is the number of degree-days required and T_min is the temperature below which the pathogen stops developing. Warming therefore shortens the incubation period sharply:

• For Plasmodium falciparum, the main cause of severe malaria (T_min ≈ 16 °C, DD ≈ 111 degree-days), development in the mosquito takes about four weeks or more at 20 °C. This is longer than most adult Anopheles mosquitoes live, so few survive to transmit. At 28 to 30 °C, development takes only about 8 to 12 days, and many more infected mosquitoes survive to become infectious.
• In Aedes aegypti carrying dengue virus, the incubation period falls from roughly 15 to 20 days at 22 °C to about 6 to 7 days at 32 °C.

Transmission does not, however, increase indefinitely with warming. At high temperatures and low humidity, vector mortality rises sharply, typically above about 32 to 34 °C, and pathogen development is impaired. Individual vector and pathogen traits therefore follow asymmetric, hump-shaped thermal performance curves, often described by the Briere function:

Combining these curves in the Ross–Macdonald framework, as in work by Erin Mordecai and colleagues, shows that transmission potential peaks at an optimum temperature (T_opt) specific to each vector and pathogen, and falls to zero above an upper limit (T_max):

Approximate thermal limits for transmission by major vectors

Temperature falls with altitude by about 6 to 6.5 °C per kilometre and also falls toward the poles. Each 1 °C of warming therefore shifts temperature zones upward by roughly 150 m and poleward by roughly 100 to 150 km. This allows vectors to reach populations with little prior exposure or immunity, both in tropical highlands, such as those of Ethiopia, Kenya, and Colombia, and at temperate latitudes. Examples include local transmission of dengue, chikungunya, and West Nile virus in southern Europe and the United States, and the spread of Ixodes ticks and of the Phlebotomus sandflies that transmit leishmaniasis.

Warmer water and soils also favour pathogens that are not spread by arthropods:

• Vibrio bacteria: salt-tolerant bacteria including Vibrio cholerae, Vibrio vulnificus, and Vibrio parahaemolyticus, which can attach to copepods, multiply rapidly when coastal sea surface temperatures exceed about 15 °C and salinity is lowered by runoff. Warming of high-latitude seas such as the Baltic has extended the range and season of V. vulnificus wound infections and shellfish-related illness. Heavy rainfall and storm surges can also overwhelm water treatment systems, contributing to outbreaks of cholera, Cryptosporidium, and pathogenic Escherichia coli.
• Environmental fungi: in the southwestern United States and northern Mexico, wet periods that promote fungal growth in soil, followed by drought and dust storms, release spores of Coccidioides into the air. This has increased the incidence and geographic range of coccidioidomycosis (valley fever). It has also been hypothesized that warming may select for fungi able to tolerate mammalian body temperature (37 °C), possibly contributing to the emergence of the multidrug-resistant yeast Candida auris.

Extreme heat is among the leading causes of weather-related death. Humans regulate their core body temperature (T_core) within a narrow range around 37 °C to maintain the structure of proteins, the properties of cell membranes, and normal cellular energy production.

Heat exchange between the body and its surroundings is described by the heat balance equation, with all terms expressed per square metre of body surface area (A_D ≈ 1.8 m² for an adult):

where:

• S is the rate of heat storage in the body. A stable core temperature requires S = 0. When S > 0, core temperature rises at a rate d_T__core/d_t_ = S A_D / (m_b c_b), where m_b is body mass and c_b ≈ 3.47 kJ kg⁻¹ K⁻¹ is the average specific heat capacity of body tissue.
• M − W is metabolic heat production minus external work. At seated rest, M ≈ 58 W/m² (about 100 W). During heavy physical labour it rises to roughly 300 to 600 W/m². Because muscles convert at most about 20 to 25% of metabolic energy into mechanical work, most of this energy appears as heat.
• C, R, and K are heat losses by convection, radiation, and conduction. Convective and radiative losses are C = h_c(T_sk − T_a) and R = h_r(T_sk − T_r), where T_sk is mean skin temperature (normally about 33 to 35 °C), T_a is air temperature, and T_r is mean radiant temperature. When air and radiant temperatures exceed skin temperature, these terms become negative and the body gains heat from its surroundings.
• E_sk is heat loss by evaporation of sweat from the skin, and C_res and E_res are small losses through breathing. Each gram of sweat that evaporates removes about 2,426 J. When the air is hotter than the skin, sweat evaporation is effectively the only way the body can lose heat.

Evaporative cooling is limited in two ways:

1. Physiological limit: the body's 2 to 4 million sweat glands can sustain sweat rates of roughly 1 to 2.5 L/h (briefly higher in heat-acclimatized individuals). If all of it evaporated, this would remove about 350 to 900 W/m². Sweat that drips off the skin provides no cooling.
2. Environmental limit: the maximum rate of evaporation is set by the difference in water vapour pressure between fully wet skin and the air:

E_max = h_e (p_sk,s − p_a) where h_e is the evaporative heat transfer coefficient, which depends on wind speed and clothing and is related to the convective coefficient by the Lewis relation (h_e/_h__c ≈ 16.5 K/kPa); p_sk,s is the saturation vapour pressure at skin temperature (about 5.6 kPa at 35 °C); and p_a is the vapour pressure of the air. The actual evaporation rate is E_sk = w E_max, where w (between about 0.06 and 1) is the fraction of the skin that is wet. In very humid air, p_a approaches p_sk,s and evaporation becomes impossible.

When warm-sensitive neurons in the preoptic area of the hypothalamus detect a rise in body temperature, the body responds with sweating and increased blood flow to the skin. Both place heavy demands on the cardiovascular system and the kidneys:

• Skin blood flow and cardiac strain: constrictor nerve activity to skin blood vessels is reduced, and sympathetic cholinergic nerves actively dilate skin arterioles. Skin blood flow can rise from about 0.2 to 0.5 L/min to 6 to 8 L/min, more than half of cardiac output. Blood pooling in skin veins reduces the return of blood to the heart, so the heart must beat faster and more forcefully to maintain blood pressure, increasing its oxygen demand. In older adults, whose cardiovascular responses are reduced, and in people with coronary artery disease or heart failure, this strain can trigger myocardial infarction, arrhythmias, and circulatory collapse. Cardiovascular causes account for most excess deaths during heat waves.
• Gut barrier failure and heat stroke: to supply the skin without a fall in blood pressure, blood vessels supplying the gut, liver, and kidneys constrict, reducing their blood flow substantially. Reduced blood flow combined with high temperature (core temperature above about 40 °C) damages the cells lining the intestine and the tight junctions between them. Bacterial lipopolysaccharide (endotoxin) can then pass from the gut into the bloodstream. There it activates Toll-like receptor 4 on immune cells and the lining of blood vessels, triggering a strong inflammatory response involving interleukin 6, interleukin 1β, and tumor necrosis factor. The resulting systemic inflammatory response syndrome, disseminated intravascular coagulation, muscle breakdown (rhabdomyolysis), brain injury, and multiple organ failure are characteristic of severe classic and exertional heat stroke.
• Dehydration and kidney disease: heavy sweating during outdoor labour, which can reach 6 to 12 litres or more per day, reduces body fluid volume and concentrates the blood. Dehydration and rhabdomyolysis can cause acute kidney injury, and dehydration increases the risk of kidney stones. Repeated heat stress and dehydration have also been linked to an epidemic of chronic kidney disease of non-traditional origin (Mesoamerican nephropathy) among agricultural workers. Its causes are still debated and may include agrochemicals and other factors. One proposed mechanism is that high blood concentration activates the polyol pathway in the kidney, producing sorbitol and fructose, whose breakdown by fructokinase depletes cellular energy, raises uric acid, and damages the kidney tubules.

Because heat loss depends on both temperature and humidity, heat stress is often measured using the wet-bulb temperature (T_w), the lowest temperature to which air can be cooled by evaporating water into it at constant pressure. The wet-bulb globe temperature (WBGT = 0.7_T__nw + 0.2_T__g + 0.1_T__a) also includes the effect of solar radiation, measured with a black globe thermometer.

In 2010, Steven Sherwood and Matthew Huber proposed a theoretical upper limit for human survival of a sustained wet-bulb temperature of 35 °C. This corresponds to 35 °C at 100% relative humidity, or about 46 °C at 50%. To lose metabolic heat from a core at 37 °C, the skin must stay below about 35 °C. A person covered in sweat behaves like a wet-bulb thermometer: if the wet-bulb temperature of the air exceeds 35 °C, the body cannot lose heat even with unlimited sweating, full shade, strong wind, and no clothing. Under these conditions, even a healthy person at rest would reach a lethal core temperature within about six hours.

Laboratory studies with human volunteers, including the Pennsylvania State University HEAT Project led by W. Larry Kenney and Daniel Vecellio beginning in 2022, have shown that the actual limit is considerably lower. Above this lower limit, even a resting person can no longer keep core temperature stable:

Critical wet-bulb temperatures for maintaining a stable core temperature

Humid coastal regions next to very warm seas, especially around the Persian Gulf and Red Sea, the Indus and Ganges valleys, eastern China, and parts of West Africa and Central America, already experience wet-bulb temperatures above 31 °C during severe heat waves. Readings above 35 °C have been recorded briefly at a few weather stations near the Persian Gulf.

Climate change worsens air quality both by speeding up the chemical reactions that produce pollutants and by increasing smoke from wildfires.

Unlike stratospheric ozone, which shields the surface from ultraviolet radiation, ground-level ozone (O₃) is a secondary pollutant that damages the lungs. It forms from nitrogen oxides (NO_x = NO + NO₂), emitted mainly by fuel combustion and soils, and volatile organic compounds (VOCs), in the presence of sunlight (wavelengths shorter than about 420 nm):

On its own, this cycle produces little net ozone, because NO destroys ozone again (NO + O₃ → NO₂ + O₂). However, when VOCs and carbon monoxide are oxidized by hydroxyl radicals, they form peroxy radicals (HO₂ and RO₂). These convert NO to NO₂ without consuming ozone (RO₂ + NO → RO + NO₂), so ozone accumulates.

Warming increases surface ozone, by roughly 1 to 5 ppb per °C in polluted regions even if emissions stay the same, an effect known as the climate penalty. Three mechanisms contribute:

1. Breakdown of peroxyacetyl nitrate: in cool conditions, NO_x is stored in the stable compound peroxyacetyl nitrate (PAN, CH₃C(O)OONO₂). PAN breaks down rapidly at high temperatures, releasing NO₂.
2. Increased isoprene emissions: many broadleaf trees emit isoprene (C₅H₈), which helps protect their leaves from heat damage. Emissions increase two- to threefold between 25 and 35 °C, adding reactive hydrocarbons to the ozone-forming reactions.
3. Stagnant air: high-pressure systems associated with heat waves bring clear skies, which increase the rate of photochemical reactions, and light winds, which trap pollutants near the ground.

Inhaled ozone reacts with fatty acids and antioxidants in the fluid lining the airways, producing reactive oxygen species that inflame the airways and make them more reactive. This worsens asthma and increases deaths from chronic obstructive pulmonary disease.

Longer growing seasons and higher CO₂ concentrations also increase the length of the pollen season and the amount of pollen produced, for example by ragweed (Ambrosia artemisiifolia), whose content of the major allergen Amb a 1 increases at high CO₂. Production of fungal spores such as Alternaria and Cladosporium also increases. Together these changes worsen allergic rhinitis and asthma.

Rising temperatures and drier vegetation are increasing the frequency and extent of wildfires, which release large amounts of fine particulate matter (PM_2.5, particles 2.5 μm or smaller in diameter) and ultrafine particles (smaller than 0.1 μm).

Larger particles (PM₁₀) are mostly trapped in the nose and upper airways. PM_2.5, by contrast, reaches the smallest airways and alveoli, and the smallest ultrafine particles may pass into the bloodstream. Several studies suggest that wildfire smoke is more harmful per unit mass than urban PM_2.5, possibly because it is rich in organic compounds, polycyclic aromatic hydrocarbons, quinones, and other reactive substances. Wildfire particles activate immune cells in the lung (including through the NLRP3 inflammasome and the NF-κB pathway), impair the function of blood vessel linings, and make blood more likely to clot. Smoke episodes are associated with increased hospital admissions for respiratory disease, stroke, and heart attack, and with adverse pregnancy outcomes such as preterm birth and low birth weight.

Global food security depends on the yields and nutritional quality of staple crops and on fisheries. Wheat, rice, maize, and soybeans together provide about two-thirds of the calories consumed by humans.

Crop development is driven by accumulated heat (growing degree-days). Warming can lengthen growing seasons at high latitudes, but across most major growing regions, rising temperatures and more variable rainfall reduce yields. Without adaptation, global yields of the major staples are estimated to fall by roughly 3 to 7% for each 1 °C of global warming.

• Heat at flowering: cereals and legumes are very sensitive to short periods of high temperature, even 2 to 5 days, during pollen formation and flowering. Above critical canopy temperatures of about 30 to 32 °C for wheat, 33 to 35 °C for rice, and 35 °C for maize, heat damages the cells that nourish developing pollen and kills pollen grains. Dry air also dries out the receptive parts of the flower, such as maize silks, preventing pollination and causing developing grains to abort. A short heat wave reaching 38 °C during flowering can leave panicles or ears almost empty, even when the rest of the season has been favourable.
• Shortened grain filling: after flowering, high temperatures speed up crop development and leaf ageing, shortening the period during which sugars are moved into the developing grain. Grain weight and yield are reduced as a result.
• Droughts, floods, and fisheries: a warmer atmosphere holds more moisture, in line with the Clausius–Clapeyron relation, so rainfall extremes intensify. Crops face both rapid-onset (flash) droughts, which close leaf pores and halt growth, and intense downpours, which waterlog soils, wash away nitrogen, and erode topsoil. In the ocean, warming and loss of oxygen are projected to reduce the potential fish catch, especially in the tropics, where many people depend on fish for omega-3 fatty acids and micronutrients. Some researchers have proposed that fish will also become smaller because larger bodies are harder to supply with oxygen, although this hypothesis is contested.

In C₃ crops, such as wheat, rice, barley, potatoes, and legumes, higher atmospheric carbon dioxide increases the CO₂ concentration inside leaves. This speeds up carbon fixation by RuBisCO and suppresses photorespiration, the CO₂ fertilization effect. However, free-air concentration enrichment (FACE) experiments, in which crops are grown in the open under elevated CO₂, have shown that crops grown at about 550 ppm CO₂ are less nutritious. This research has been synthesized by Irakli Loladze, Samuel Myers, Arnold Bloom, and others. Compared with crops grown at current CO₂ levels, C₃ grains and tubers show:

• about 6 to 15% less protein;
• about 5 to 10% less iron and zinc, along with reductions in magnesium, calcium, copper, and sulfur;
• in rice, about 13 to 30% less of several B vitamins (thiamine, riboflavin, pantothenic acid, and folate), although vitamin E increases.

Several mechanisms contribute to these changes:

Proposed mechanisms of nutrient decline under elevated CO₂

How much of the zinc and iron in grains the body can absorb depends partly on phytic acid (phytate), the main storage form of phosphorus in seeds. Phytate binds zinc and iron in the small intestine, and humans produce little of the enzyme (phytase) needed to break it down. Zinc absorption is markedly reduced when the molar ratio of phytate to zinc in the diet exceeds about 15. Lower zinc in grains could raise this ratio, although phytate itself also declines under elevated CO₂ in some crops.

About two billion people obtain at least 60% of their dietary zinc or iron from C₃ crops, mostly in South Asia, Africa, and the Middle East. In these populations, CO₂-driven declines in grain quality could worsen "hidden hunger": iron-deficiency anemia, which impairs maternal health and child development; zinc deficiency, which weakens immunity and gut integrity and slows child growth, increasing vulnerability to diarrhoea and respiratory infections; and protein undernutrition.

• Heat illness
• Planetary health
• Climate change and infectious diseases
• Air pollution