Rising atmospheric carbon dioxide may already be leaving a measurable imprint inside the human body, according to a study analyzing more than two decades of US health data, which found blood bicarbonate levels have climbed roughly 7% since 1999 in a pattern that closely tracks the rise in atmospheric CO2, while calcium and phosphorus levels have simultaneously declined.
What Happened
The study, published in the journal Air Quality, Atmosphere & Health by researchers Alexander Larcombe of Curtin University and Phil Bierwirth, an emeritus geoscientist affiliated with the Australian National University, analyzed blood chemistry data from the US National Health and Nutrition Examination Survey, which collected samples from roughly 7,000 Americans every two years between 1999 and 2020. The researchers compared trends in three specific blood markers, bicarbonate, calcium, and phosphorus, against atmospheric CO2 measurements recorded at the Mauna Loa Observatory over the same period.
Average blood bicarbonate concentrations rose from 23.8 to 25.3 milliequivalents per liter over the study period, an increase of about 7%, or roughly 0.34% annually, closely paralleling the rise in atmospheric CO2 from about 369 parts per million in 2000 to more than 420 parts per million today. Over the same period, average blood calcium levels declined by roughly 2%, and phosphorus levels fell by approximately 7%.
If current trends continue, the researchers’ modeling suggests average bicarbonate levels could approach the upper limit of today’s accepted healthy range within about 50 years, while calcium and phosphorus could reach the lower end of their healthy ranges by the end of the century. The researchers noted the findings may be particularly relevant for children and adolescents, whose developing bodies face the longest cumulative lifetime exposure to rising atmospheric CO2.
Why It Matters
Humans evolved in an atmosphere containing roughly 280 to 300 parts per million of CO2 for at least the 150,000-year history of Homo sapiens, according to the fossil record, a level that remained relatively stable until recent decades, when it began rising dramatically due to human greenhouse gas emissions. The researchers’ central hypothesis is that human physiology may not be fully adapted to sustained exposure to CO2 levels this far outside that historical range.
In the body, CO2 is converted into bicarbonate, a compound that plays an important role in maintaining healthy blood pH levels. As CO2 rises, kidneys can retain additional bicarbonate to help keep blood pH stable, while bones can also buffer excess acidity by releasing minerals like calcium and phosphorus, a process that, if sustained chronically over long periods, researchers say could potentially affect bone strength and mineral balance over time.
Study co-author Bierwirth said the consistency of the population-wide trends across the two-decade dataset is difficult to dismiss, even though the study does not establish direct causation. “It appears we are adapted to a range of CO2 in the air that may now have been surpassed,” he said, adding that the findings suggest reducing CO2 emissions may be important not just for climate stability but for safeguarding long-term human health as well.
Context and Background
The researchers specifically selected bicarbonate, calcium, and phosphorus as study markers because of their well-established role in the body’s acid-base buffering system, theorizing that population-level shifts in these markers over time could serve as a biological tracer of sustained atmospheric CO2 exposure, an approach the researchers describe as a novel application of the NHANES dataset, which they characterize as the most comprehensive blood chemistry dataset available for this kind of long-term population analysis.
The average annual increase in atmospheric CO2 has been roughly 2.6 parts per million over the past decade, with 2024 alone recording a 3.5 parts-per-million increase, reflecting an accelerating rather than steady rate of atmospheric change that, if the study’s hypothesized mechanism holds, could translate into an correspondingly accelerating rate of blood chemistry change in the coming years.
The study’s authors acknowledge important limitations, noting that their analysis did not account for other factors that could independently influence blood chemistry trends over the same period, including changes in population diets, medication use, kidney function, rates of obesity, or the amount of time people spend indoors, where CO2 concentrations tend to run considerably higher than outdoor levels.
Expert Analysis
Larcombe emphasized that despite the consistency of the population-level pattern, “we can’t say for certain that these changes that we’re seeing are 100% due to climate change,” underscoring that the relationship identified in the study remains correlational rather than a proven causal mechanism, a distinction the researchers stress is important for accurately interpreting the findings.
The study’s authors argue that even without definitive proof of causation, the consistency and scale of the observed pattern across a large, nationally representative population dataset warrants including potential physiological effects of rising atmospheric CO2 as part of future climate policy discussions, expanding the conversation beyond CO2’s role in driving climate change to include its potential direct effects on human biology.
Outside researchers reviewing the study’s broader implications note that chronic, low-level shifts in blood chemistry of the kind identified could theoretically compound with other established environmental health stressors, though they caution that translating population-level statistical trends into specific individual health risk predictions requires considerably more research before firm clinical conclusions can be drawn.
What Happens Next
The study’s authors are calling for expanded monitoring that tracks atmospheric CO2 composition alongside biological markers across populations over time, arguing that such tracking should become a standard component of future climate and public health policy discussions rather than being treated as a separate, unrelated area of research.
Given the study’s identified limitations, including its inability to fully account for confounding factors like diet and indoor CO2 exposure, further research incorporating those variables is likely needed to more definitively establish whether the observed blood chemistry trends are directly attributable to atmospheric CO2 levels specifically, a question the study’s authors identify as a clear priority for future investigation.
