Extreme heat may speed up aging

New research in links rising outdoor temperatures to accelerated biological aging, raising urgent concerns about climate change’s impact on health.

Study: Ambient outdoor heat and accelerated epigenetic aging among older adults in the US. Image Credit: Bartolomiej Pietrzyk / Shutterstock.com

A recent Science Advances study determines the role of ambient outdoor heat in epigenetic aging.

Extreme heat and biological aging

Due to global warming, the intensity, frequency, and duration of extreme heat events will continue to increase over the next several decades, with the negative health effects of extreme heat particularly evident among older adults. To date, it remains unclear how extreme heat may impact morbidity and mortality.

Previous in vivo studies suggest that extreme heat stress may induce ‘maladaptive epigenetic memory,’ which can be characterized by changes in DNA methylation (DNAm) patterns. In addition to these alterations in the DNA methylome, extreme heat may also induce phenotypic changes; however, limited studies have explored this potential association.

Several studies have reported the effects of heat on DNAm across different species. For example, one extreme heat stress episode can lead to durable changes in DNAm in mice, with various cells and tissue types affected.

About the study

The researchers of the current study examined the role of ambient outdoor heat in epigenetic aging using data from a nationally representative sample of older adults residing in the United States. Blood samples were collected at various time points to determine whether epigenetic aging responds to both acute and chronic heat in the outdoor home environment. The role of sociodemographic differences in these associations were also studied.

A heat index (HI) was used as a measurement of heat, as this value considers temperature and humidity to reflect what the human body actually feels. DNAm was assessed from peripheral blood cell DNA based on DNAm epigenetic age measures of PhenoAge, GrimAge, and DunedinPACE.

Study findings

Heat levels were classified as caution level or higher, extreme caution level or higher, and danger level or higher. Individuals with area-level caution+ heat on the day of their blood collection exhibited an increase in the rate of PCPhenoAge changes that equated to 1.07 years.

The PCPhenoAge acceleration over a seven-day period was 1.15 years for every unit increase in heat days at the caution+ level. The association between heat days and the rate of PCPhenoAge acceleration remained significant over 30 days, one-year, and six-year periods. Comparable results were recorded for heat days at the extreme caution+ level.

Significant heat effects were observed for longer time periods for both PCGrimAge and DunedinPACE. A single unit increase in heat days at the caution+ level was associated with a 3% faster rate of DunedinPACE changes and 0.62-year increase in PCGrimAge acceleration over one year.

Over six years, the rise in DunedinPACE was 5% faster and the increase in PCGrimAge acceleration was 1.09 years for every unit increase in extreme caution+ heat days. These associations were insignificant for short- and medium-term horizons.

The relationship between ambient heat and epigenetic aging was assessed across key sociodemographic subgroups including race/ethnicity, age, gender, education, and wealth. When these factors were considered, the observed patterns were largely consistent across subgroups. No strong evidence for heightened vulnerability within specific sociodemographic groups was observed.

The associations between ambient heat and epigenetic aging were robust in a series of sensitivity analyses. Consistent associations were recorded while using mean HI calculated from daily relative humidity and mean air temperature, as well as when average continuous HI values were used as a linear term in the regression models.

These findings were also consistent when the effect estimates at the 25^th percentile of the number of heat days at the caution+ level was compared to the 90^th percentile using natural cubic spline models.

Prolonged ambient heat can drive more persistent and extensive changes in physiological deterioration that accumulate over time and are reflected in accelerated biological aging.”

Conclusions

The current study provides new insights into the different biological mechanisms involved in the relationship between ambient heat to age-related morbidity and mortality risks. Overall, these results indicate that epigenetic aging can be significantly accelerated by short-, mid-, and long-term ambient outdoor heat.

Taken together, the study findings have implications for developing mitigation strategies against climate change and targeted public health interventions to reduce the adverse biological effects associated with exposure to extreme heat.