Article URL: https://link.springer.com/article/10.1007/s11869-026-01918-5 Comments URL: https://news.ycombinator.com/item?id=48949255 Points: 31 # Comments: 15
Anthropogenic activities are increasing the amount of carbon dioxide (CO2) in the atmosphere. There is mounting experimental evidence that lifetime exposure to these increasing atmospheric CO2 levels can negatively impact the normal physiology of organisms. However, directly assessing this in humans is very difficult. We analysed serum bicarbonate (HCO3−), calcium (Ca) and phosphorus (P) levels from the U.S. National Health and Nutrition Examination Survey (NHANES) from 1999 to 2020 as indirect proxies for atmospheric CO2 exposure. Over this period, average bicarbonate levels in this population show an increasing trend which parallels rising atmospheric CO2 concentrations. Both Ca and P have decreased steadily over the same period. If these trends continue, blood bicarbonate values could be at the limit of the accepted healthy range in half a century, and Ca and P will be at the limit of their healthy ranges by the end of this century. Studies indicate that, after this time, elevated atmospheric carbon dioxide, leading to CO2 accumulation in the body, has the potential to cause a range of adverse health effects. These findings highlight the urgent need for significant reductions in anthropogenic CO2 emissions to safeguard public health.
In aerobic organisms, including humans, CO2 is produced as a by-product of cellular respiration and needs to be removed from the body as a waste product via expiration (Raven et al., 2007). CO2 crosses the cell plasma membrane, enters the blood and almost all of it (90–95%) diffuses into the red blood cells, where it is rapidly hydrated to hydrogen (H+) and bicarbonate (HCO3−) by the enzyme carbonic anhydrase (CA) (Arlot-Bonnemains et al., 1985; Lan et al., 2025). HCO3− in blood is the most important means of transport for CO2 throughout the body (Sherwood, 2013) and when that blood reaches the lungs, the reaction is reversed. HCO3− in the lungs combines with H+ produced by the oxygenation of deoxyhemoglobin to produce water and CO2, which is exhaled as a waste product (Lan et al., 2025). Carbonic anhydrase thus allows a large pool of otherwise slowly reacting plasma HCO3− to be utilized in CO2 excretion (Arlot-Bonnemains et al., 1985). A quantitative relationship exists between plasma HCO3− and levels of CO2, in the blood whereby when CO2 increases, so does HCO3− and vice versa. This is evident in multiple clinical situations (Martinu et al., 2003; Ueda et al., 2009). Importantly, abnormal CO2 retention, or impaired CO2 elimination, which is seen in diseases (Mendez et al., 2019; Palmer & Clegg, 2023), impaired ventilation, or excessive CO2 inhalation (Robertson, 2006), can result in reduced blood pH. The body then attempts to buffer this ‘acidosis’ by various mechanisms, including increased ventilation (if possible), increased renal excretion of acid and conservation of filtered HCO3− (Sherwood, 2013), retention of calcium, phosphates and other substances (Gray et al., 1973) and nervous system stimulation to counteract the direct effects of pH changes on heart contractility and vasodilation (Burton, 1978; Eckenhoff & Longnecker, 1995). Calcium and phosphate (PO₄³⁻) play important supporting roles in maintaining blood acid-base balance, working alongside the HCO3− buffer system. Phosphate can accept or donate hydrogen ions to help stabilize pH, and when blood becomes acidic, calcium and phosphate can be released from bone to help neutralize excess acid (Salcedo-Betancourt & Moe, 2024).
This leads to the question as to whether increases in atmospheric CO2 pose a threat to human health. There are now many studies that review health effects in the range 600–5,000 ppm CO2 (Azuma et al., 2018; Bierwirth, 2025; Carr et al., 2025; Jacobson et al., 2019) although there is still a paucity of studies investigating the effects of long-term exposure at relevant levels of CO2. As such, the U.S. National Health and Nutrition Examination Survey (NHANES) study, which recorded blood chemistry parameters, such as HCO3−, calcium (Ca), and phosphorus (P), from about 7,000 people every two years between 1999 and 2020, provides a unique opportunity to assess potential secular trends in human blood biochemistry that may be a result of a changing air composition.
The ancestor of modern humans is thought to have evolved between 5 and 8 million years ago, with the first Homo sapiens appearing in the fossil record around 150,000 years ago (Wood, 1996). Although not precise, it appears that throughout most, if not all, of the ensuing period of human evolution, levels of CO2 in the atmosphere remained relatively stable around 300 parts per million (ppm). These data were derived from a combination of studies of relict features including air trapped in ice cores (Barnola et al., 1987), the composition of fossil plankton (Zachos et al., 2001) and Carbon-13 (13C) content in fossil plant material (Cui et al., 2020). However, since the advent of widespread industrialisation, atmospheric CO2 levels have exponentially increased (Fig. 1). In just the last ~ 50 years it has risen from < 340 ppm (in 1980), to > 420 ppm in 2025 (Lan et al., 2025). Atmospheric CO2 is currently increasing at more than 2 ppm each year, largely due to humanity’s activities, such as the burning of fossil fuels (Eggleton, 2012).
Atmospheric carbon dioxide concentrations (in ppm) over the last 800,000 years, based on measurements of air trapped in Antarctic ice (Lüthi et al., 2008; Rubino et al., 2019), and direct measurements made at the Mauna Loa Observatory (1958 to present) (Keeling et al., 2005)
As levels of atmospheric CO2 increase, it is obvious that humans will have no option but to inhale more CO2. It is also known that increased blood loading with CO2 (hypercapnia) is physiologically correlated with HCO3− levels (Malte & Wang, 2024), due to the hydration of CO₂ to form carbonic acid, which dissociates into H⁺ and HCO₃⁻. To compensate, renal mechanisms increase HCO₃⁻ reabsorption and generation to buffer H⁺ and partially restore pH homeostasis (Alka & Casey, 2014). This potentially represents a health risk if HCO3− levels increase above the normal healthy range and/or the duration of increased HCO3− is excessive. In healthy adult humans, arterial HCO3− is typically between 22 and 26mEq/L (Larkin & Zimmanck, 2015), although a recent re-evaluation suggests that 22.1–28.3mEq/L is more appropriate for arterial blood, and up to 30mEq/L is appropriate for venous blood (Kraut & Madias, 2018).
Although temporal population biochemical data relating to HCO3− are rare, a previous study (Zheutlin et al., 2014) examined data from the U.S. National Health and Nutrition Examination Survey (NHANES) from 1999 to 2012 (7 cycles) looking at the population average HCO3− levels in blood samples from a total of 33,546 adults (~ 5,000 per cycle). Between 1999 and 2012, there was an upward trend in serum HCO3− levels in the study population, with it increasing approximately 5%, from ~ 23.8mEq/L in 1999–2000 to ~ 25.0mEq/L in 2011–2012. This increase paralleled atmospheric CO2 levels which increased by a similar proportion over the same period (from ~ 369ppm to ~ 393ppm) (Lan et al., 2025). The authors question whether “the increasing trend in serum bicarbonate found in our study is related to elevated ambient CO2 and climate change”.
The overarching NHANES protocol is ethically approved by the Ethics Review Committee of the National Center for Health Statistics, which involved obtaining informed consent from all participants. The NHANES project assesses health and nutrition in a representative sample of adults and children in the United States via interviews, physical examinations and laboratory tests.
