Climate change and clinical biochemistry

The existence of direct and specific links between climate change and clinical biochemistry is not obvious. Climate change is overwhelmingly over-arching, with actual and potential impacts on every facet of human existence. In this context, teasing out specific connections with our specialty may appear self-referential at best. It is not even obvious where to look; the yield from the usual search engines and libraries provides thin gruel. However, several recent publications provide a basis for examining the links and posing the question.

First, October 2022 saw the publication of the latest annual report of the Lancet Countdown on health and climate change. ¹ This is one of a series of initiatives that seeks to join the dots between climate change and human health, and styles itself as the only independent monitoring mechanism for climate and health. The findings of the latest report predictably make for grim reading. As the accompanying editorial puts it, ‘the world is edging closer to multiple tipping points that, once crossed, will drive temperature change well above 2°C’. ² Specific attention is drawn to extreme weather events and their direct consequences, especially on vulnerable populations, and economic impact, including food insecurity and instability. Climate change is also implicated in the spread of infectious diseases, with malaria, dengue and Vibrio pathogens all getting specific mention. The Countdown report is helpful and depressing in equal measure. Its scope is so enormous that although it provides a detailed and useful ‘report card’ on the status quo in relation to various indicators, it cannot be expected to drill down to additional levels of detail.

Such additional details is available for some diseases or groups of diseases, but it is patchy. A difficulty that immediately presents itself is how to assess the extent to which a disease or set of diseases is attributable to climate change? The World Health Organization provides a structured framework for this: Driving Force, Pressure, State, Exposure, Effect and Action (DPSEEA). ³ This is useful in ensuring that nothing major is forgotten and, importantly, includes protective and corrective actions. But even where this is applied, say, to cardiovascular diseases, ⁴ the models are complicated. For example, it can readily be appreciated that exposure to extreme temperatures and poor air quality promote inflammation, hypercoagulability, fluid depletion and electrolyte imbalances, and that these in turn can be expected to translate directly into cardiovascular events. Indeed, there is a sizeable body of evidence that air pollution influences cardiovascular morbidity and mortality. However, extreme temperatures are usually relatively short term compared with air pollution. There are ways of studying these, for example, case-crossover studies, ⁵ but the health effects of seasonal or yearly temperature patterns are less widely studied. Despite detailed mechanistic insights into how climate change may exacerbate or contribute to the development of cardiovascular disease, the conclusion, almost inevitably, is that the interaction between climate change and health outcomes is diverse and complex, ranging from direct effects of abnormal temperatures on body physiology to indirect effects on infrastructure and social determinants of health. Similar considerations apply to other chronic diseases that have received attention.

Where does clinical biochemistry fit into all of this? As part of the health service, it and other pathology disciplines contribute to climate change. One estimate attributed 4.4% of annual carbon dioxide emissions to the health services of 36 major countries; predictably, hospitals were the main sources. ⁶ At the very least, this should prompt us to focus on our own carbon dioxide emissions. The second recent article of interest has done precisely that. ⁷ The authors, from Australia, estimated the carbon footprint (assessed as carbon dioxide equivalent emissions or CO₂e) of full blood count examination, urea and electrolytes, coagulation profile, C-reactive protein and arterial blood gases. The importance of this study lies at least partly in the novelty of its application. It used an established methodology, called life cycle assessment, that estimates the footprint of a product or service through its entire life cycle, from raw material extraction to waste disposal and recycling. The international standard for life cycle assessment has already been applied to other parts of the health service, for example, anaesthetic drugs and surgical procedures, but this is the first study to apply it to pathology testing. (The study used a consequential approach, measuring the marginal or incremental impact of individual tests, rather than an attributional approach). Sample collection and phlebotomy were the major contributors to the footprint, while emissions due to laboratory power use and reagents were much smaller. As the authors point out, the carbon footprints of individual tests were small, but their cumulative impact significant. There is limited scope for reducing the footprint from improving the energy efficiency of analysers, using electricity from renewable sources, etc.; changing the behaviour of clinicians is likely to be the most effective way to reduce it. The acknowledged limitations of the study (having to make assumptions about manufacture of phlebotomy equipment and reagents, in the absence of primary data) are minor, and it is sufficiently detailed to serve as a useful model for others wishing to do similar studies.

Which brings us to the final paper of interest, published in this issue of the Annals. ⁸ This Belgian study began as an investigation into unacceptable assay instability in the measurement of total CO₂. It broadened into a deeper investigation of the effect on total CO₂ measurement of atmospheric CO₂ within the internal laboratory environment, that included documenting atmospheric CO₂ concentrations and their correlation with assay performance. Relevant weather data, for example, wind speed, that might affect laboratory ventilation, were also retrieved. The conditions of assay measurement were varied by opening ventilation grids next to the windows and strictly enforcing the closure of reagent chamber lids in accordance with good laboratory practice. Their main conclusions – that fluctuations in atmospheric CO₂ affect the measurement of total CO₂ and that the assay environment can be made more stable by improving ventilation and closing chamber lids – are not surprising. Equilibration of CO₂ in the air and in the sample is well-recognised as a source of error in total CO₂ measurement. But the detail of recording, and the experimentation with relevant factors like ventilation, allowed them to draw a broader conclusion – that the prevailing atmospheric CO₂ can affect measurement of total CO₂ systematically. Although the findings relate specifically to CO₂ in the internal laboratory environment, they offer a ‘proof of principle’ that (external) environmental CO₂ could have a similar effect. Here, then, is a direct and specific link between climate change and clinical biochemistry.

What of the future? What practical steps can we take to minimise the carbon footprint of clinical biochemistry? In the short term, the findings of the carbon footprint study discussed above should be replicated and extended, with data being collected routinely. This will simultaneously strengthen the evidence base and act as an ongoing reminder of the need for change. Initiatives that seek to reduce unnecessary investigations, for example, Choosing Wisely^{® 9} and national minimum retesting intervals in pathology, ¹⁰ should be embraced and implemented widely. Looking further forward, investigations, particularly those related to monitoring, are likely to be subject to increasing scrutiny in the years ahead. Clinical biochemists – and clinicians – should prepare for a time when justification of the need for investigation will become increasingly routine.