• Nicotinamide adenine dinucleotide (NAD+) levels fall 39.86% in the lungs from air pollutant (particulate matter [PM]) exposure, likely inducing inflammation that precipitates lung injury
  • Supplementing with nicotinamide mononucleotide (NMN) before and during PM exposure prevents damaging lung injury.
  • Confirming NMN’s lung-preserving effects against inflammation, NMN supplementation cuts in half elevated inflammatory protein TNF-ɑ levels from PM exposure.

Numerous people live with air pollution in the forms of solid particle and liquid droplet mixtures from sources like car exhaust and factory fumes, especially those in urban environments. With 80% of the US population living in cities, high numbers of people inhale these miniscule mixtures of solids and liquids called particulate matter (PM). Over years of exposure to them, effects range from lung injury to immunosuppression. Nutrient supplementation with probiotics, vitamins C and E, and other antioxidants have been proposed to mitigate PM exposure’s effects, but researchers note that more efficient remedies to thwart progressive lung injury are needed.

Published in Environmental Health Perspectives, Chen and colleagues from Sun Yat-sen University in China show that PM exposure dramatically reduces lung NAD+ levels, which likely contributes to inflammation and lung injury in mice. Supplementing with NAD’s precursor, NMN, has been shown to restore NAD+ levels, and the researchers demonstrated that NMN supplementation prevents severe lung injury with PM exposure. The researchers go on to confirm that NMN prevents severe lung injury by alleviating inflammation as it reduces levels of the inflammatory protein TNF-ɑ with PM exposure. These results support that NMN supplementation mitigates lung injury and systemic inflammation from PM exposure, which is especially helpful for those living in urban environments.

NMN Prevents Air Pollutant-Induced Lung Injury and Curtails Inflammation

To find whether PM exposure affects NAD+ levels to drive inflammation and subsequent lung injury, Chen and colleagues subjected mice to a chamber with high levels of PM for 16 weeks. After the PM exposure regimen, the researchers measured NAD+ levels in different tissues. They found that NAD+ levels dropped 39.86% in the lungs, 37.28% in the liver, and 41.20% in the spleen. These findings provide evidence that PM exposure’s harmful effects on the lungs can be at least partially attributed to lower NAD+ levels.

(Zhang et al., 2023 | Environmental Health Perspectives) Sixteen weeks of PM exposure drastically reduces NAD+ levels in different tissues. With PM exposure (Exp), NAD+ content drops 39.86% in the lungs, 37.28% in the liver, and 41.20% in the spleen compared to healthy, unexposed mice (Con).

Since NMN supplementation has been shown to increase NAD+ levels, Chen and colleagues sought to find whether administering NMN in drinking water (500 mg/kg/day) alleviates PM-induced lung injury. The researchers began NMN supplementation two weeks before PM exposure (18 weeks total) and found NMN prevents severe PM-induced lung injury. These findings suggest that NMN supplementation thwarts lung injury from PM exposure.

(Zhang et al., 2023 | Environmental Health Perspectives) NMN prevents acute lung injury (ALI) in PM-exposed mice. ALI scores were calculated based on parameters like protein debris in the lungs and the prevalence of immune cells present. PM exposure almost doubled ALI scores, indicating increased lung injury, but NMN significantly prevented this substantially increased ALI score.

The China-based researchers sought to confirm that NMN alleviates PM-induced lung injury by mitigating inflammation. They measured blood plasma inflammatory protein TNF-ɑ levels and found that PM exposure more than doubled TNF-ɑ content. NMN treatment cut the elevated TNF-ɑ levels in half. These data support that NMN increases NAD+ to inhibit inflammation that can lead to lung injury.

(Zhang et al., 2023 | Environmental Health Perspectives) NMN prevents the drastic accumulation of protein markers for inflammation. PM exposure (Exp) more than doubled blood plasma levels of the protein marker for inflammation TNF-ɑ. NMN nearly cut the PM-induced TNF-ɑ levels in half.

“These novel findings provide new insights into effective intervention strategies for dietary nutritional supplements and protection of human health, specifically lung injury, against adverse environmental stimuli,” said Chen and colleagues.

Using NMN to Preserve Lungs Against Air Pollutants

The study showed that NAD+ levels significantly drop after extended durations of PM exposure, which typically precipitates inflammation. Inflammation leads to tissue damage, namely, lung damage with PM exposure. NMN effectively mitigated lung injury from PM exposure, likely by decreasing inflammation.

Another study also showed that NMN protects skin cells against PM-induced damage. The data from Chen and colleagues showing NMN prevents lung damage from air pollutants along with the skin cell aging study provide evidence that NMN protects multiple organ systems against environmental pollutants.

The study has a few limitations. For example, Chen and colleagues could have confirmed that PM exposure-induced falling NAD+ levels were increased with NMN treatment. However, the research team only showed that NAD+ levels fall with PM exposure and assumed that NMN would rescue NAD+ levels.

Future clinical research can verify whether daily NMN supplementation prevents lung injury in urban-dwelling humans. Positive findings would mean that people can increase NAD+ levels with NMN to prevent inflammation and lung injury associated with air pollutants.