News from the 90th EAS Congress, Milan Italy
Science cannot provide all the answers to improving our health: we also need to be proactive in targeting our environment.
According to the World Health Organization, in 2016, about one-quarter of all deaths worldwide were attributable to the environment.1 Understanding how much of this burden of disease can be attributed to modifiable environmental risks can help in identifying opportunities for prevention and add impetus to global efforts for policy change. Despite accumulating data, however, the relationships between health and the environment have largely remained at the periphery of global health discussions. This needs to change, especially in the light the 2030 Agenda for Sustainable Development, which highlights critical links between the environment, human well-being and the rights to life and health.
According to Dr. Sanjay Rajagopalan (Harrington Heart and Vascular Institute, University Hospitals Cleveland Medical Center, and Case Western Reserve University School of Medicine, Cleveland, Ohio, USA), attitudes to improving the environment mirror those for improving cardiovascular health with a myopic emphasis on treatment rather than prevention. The evolution of the urban environment clearly reflects this, representing the source of >50% of air pollution globally. An increasingly unhealthy urban environment increases cardiometabolic risk factors and outcomes2; in contrast, increasingly ‘greening’ cities favours all-cause mortality prevention. Urban design needs to improve the walkability, air/noise pollution, greenery and access to create ‘healthy cities’3 all of which favourably impact cardiovascular health.
Dr Thomas Münzel (Medical Center of the Johannes Gutenberg University, Mainz, Germany) discussed environmental stressors such as air and noise pollution, artificial light at night and climate change which contribute to an increasing burden of cardiovascular disease and overall mortality.4 These factors are also intensified in an urban environment. With respect to air pollutants, the smaller the particle the more likely that it will be taken up into the vasculature, promoting endothelial dysfunction, inflammation and atherosclerosis. Moreover, air pollution also triggers the development of cardiovascular risk factors such as hypertension and hypercholesterolaemia. To mitigate these effects there is a clear case for lower air pollution limits and phasing out of fossil fuels. A healthy city design with more greenspace is crucial, especially given increasing urbanisation globally.
Social vulnerability also impacts health outcomes, as discussed by Dr Khurram Nasir (Houston Methodist DeBakey Heart & Vascular Center, Weill Cornell College of Medicine, Houston Methodist Academic Institute, USA). Economic deprivation together with poor socio-cultural integration and/or ethnicity increases social vulnerability, meaning that vulnerable individuals are less likely to maintain good health, or when sick, are less likely to access treatment. This social inequity is even greater when physical disability is added to socio-economic barriers. The increasing gap between the wealthy and economically deprived has widened disparity in cardiovascular risk factors, and their management and outcomes. This extends to the use of foundational preventive treatments such as statins; US data over the period 2002-2013 highlighted lower use of statins across subgroups in women, racial/ethnic minorities, and the uninsured indicative of health care disparities.5
Finally, there is evidence that the individual’s genetics influences the response to the environment, as discussed by Dr Ruth Loos (University of Copenhagen, Denmark and Icahn School of Medicine at Mount Sinai, New York, USA). Obesity is a serious public health challenge that accounts for an increasing proportion of the global non-communicable disease burden. According to the NCD Risk Factor Collaboration, the prevalence of obesity has tripled since 1975.6 Accumulating evidence indicates that genetic predisposition to obesity can be attenuated or exacerbated by the environment. To date, however, candidate gene and genome-wide association studies have identified few loci which influence the association of body mass index/obesity and environmental factors, to allow for personalised recommendations based on genotype at this time.
References
1. World Health Organization. Estimating environmental health impacts. https://www.who.int/activities/environmental-health-impacts
2. Al-Kindi S, Rajagopalan S, et al. J Am Coll Cardiol 2022 (in press).
3. World Health Organization. What is a healthy city? ttps://www.euro.who.int/en/health-topics/environment-and-health/urban-health/who-european-healthy-cities-network/what-is-a-healthy-city
4. Münzel T, Hahad O, Sørensen M et al. Cardiovasc Res 2021; doi: 10.1093/cvr/cvab316.
5. Salami JA, Warraich H, Valero-Elizondo J, et al. JAMA Cardiol 2017;2:56-65.
6. NCD Risk Factor Collaboration (NCD-RisC). Lancet 2017;390:2627-2642.
