How nutritional interventions can be used to reduce the ill-effects of PM2.5 particulate pollution

Air pollution is a global problem with far-reaching consequences. Fine particulate matter known as PM2.5 increases the risk of illness and mortality from non-communicable diseases, especially cardiovascular and respiratory diseases. The supplementation of micronutrients with antioxidant capabilities such as vitamins B, C, E and marine omega-3 fatty acids has been shown to offset some of the worst effects of PM2.5 inhalation.

Air pollution is a global problem with far-reaching consequences. Exposure to air-borne pollutants has been associated with increased rates of cardiovascular and respiratory morbidity and mortality throughout the world. The risk increases markedly in urban areas where concentrations of pollutants are usually higher. There is considerable variability in the toxicity of the many types of pollutants, and the extent of susceptibility to their effects varies widely between individuals.

Dr Fernando Holguin, Associate Professor of Medicine in the Division of Pulmonary, Allergy and Critical Care at the University of Pittsburgh Medical Centre in the USA, said at a recent conference in Valencia, Spain (2), that “the rising exposure to pollutants is associated with increased rates of cardiovascular and respiratory afflictions worldwide. The variation in associated risk between different pollutants provides huge challenges to the legislation and development of adequate industrial production regulation. Therefore, protection strategies for people who are more vulnerable and most highly exposed must be highlighted as a necessary target.”

The fine particulate matter present in polluted air unfavorably changes the levels of inflammatory biomarkers and reactive oxygen species. Such changes increase the risk of illness and mortality from non-communicable diseases, especially cardiovascular and respiratory diseases.

Whilst the levels of some pollutants have fallen significantly in recent years, for example, lead, carbon monoxide, sulfur dioxide and nitrous oxide, the levels of particulate matter with an aerodynamic diameter less than 2.5 mm (known as PM2.5) have remained stubbornly high. PM2.5 is a complex mix of many liquid and solid components, but crucially their small size means they can be absorbed deep into lung tissue and beyond. The Global Update of Air Quality Guidelines (AQG) of the World Health Organization published in 2005 recommended that the levels of PM2.5 in the air should be maintained at an annual mean level of 10 μg/m3 and a 24 hour mean of 25 μg/m3. Further exposure to levels in excess of 35 μg/m3 lead to an increased mortality risk of 15% when compared with the recommended limit of 10 μg/m3 (annual mean).

The inhalation of PM2.5 particulates deep into lung tissue causes the body to react both locally and systemically. They cause an increased inflammatory response and decreased antioxidant ability. The reduced antioxidant ability means that the body is less able to deal with the many reactive oxygen species (ROS) generated during normal metabolism, leading to an overall increase in oxidative stress (1). PM2.5 inhalation induces cardiovascular damage, including endothelial dysfunction, reduced levels of heart rate variability (HRV) and increased levels of atherosclerosis (3,4). Not surprisingly, PM2.5 also causes structural damage to the lungs and it has been demonstrated that there is an increased risk of lung cancer (1).

It seems reasonable to hypothesize that improved nutrition could offset some of the worst effects of PM2.5 inhalation. A study of pregnant women exposed to high levels of PM2.5 in Poland showed that those participants with the highest serum levels of vitamin A produced babies of normal birth weight, whereas those with lower levels produced infants of low birth weight (5).

Vitamin C (ascorbic acid) has been shown to reduce genetic damage in humans by preserving the structure of DNA (6). Increased serum vitamin C levels decreased DNA strand breakage caused by air pollution. Oxidative damage was reduced in groups exposed to PM2.5 but supplemented with vitamin C, with their vitamin C plasma levels exceeding 50 μmol/l. A recent study (7) confirmed that PM2.5 elevated ROS generation, inhibited mitochondrial gene expression and raised levels of inflammatory cytokines in human bronchial epithelial cells. However, the addition of vitamin C to the cells strikingly reduced those PM2.5 toxic effects.

High PM2.5 levels in Mexican cities have led to children with abnormal endothelial function and vitamin D deficiency (8). In a study with residents of a nursing home in Mexico City, PM2.5 was found to suppress levels of the biomarkers Cu/Zn superoxide dismutase and glutathione which are normally produced in response to oxidative stress (9). Supplementation with fish oil (which is well-known to have anti-inflammatory properties) was able to increase levels of both biomarkers and was thus protective against PM2.5 exposure.

During the 1990’s, a link was established between PM2.5 and reduced heart rate variability (HRV). HRV is a measurement of interval oscillations between consecutive heartbeats, reflecting beat-to-beat control in the heart by autonomic regulation (1). reduced HRV is often a precursor of adverse cardiovascular outcomes, including arrhythmia, heart attacks and sudden cardiac death. When a daily 2 g intervention of fish oil was given to the residents of the nursing home in Mexico City mentioned earlier (and who were exposed to PM2.5), it was able to prevent the decline in HRV in the treatment arm (10). In another trial, 20 healthy middle-aged subjects were randomly assigned to receive either 3 g fish oil or placebo every day for four weeks (11). The subjects were then placed in an experimental chamber where they were exposed to high concentrations of PM2.5 (average 278 µg/m3). The HRV reduced drastically in the placebo group and maintained that level for 20 hours, whereas the fish oil group were largely unaffected.

It has also been shown that dietary methyl nutrients, including folate, vitamin B6, vitamin B12 and methionine may help prevent the HRV reduction associated with PM2.5 exposure. A protective effect of methyl nutrients was shown in the elderly male participants of the Normative Aging Study (12), though it has to be noted that this was not a randomized, blinded clinical trial. PM2.5 particularly affects those with genetic polymorphisms associated with methylene tetrafolate reductase (13). It seems reasonable to suggest that B vitamins and other methyl nutrients would be particularly beneficial to maintaining HRV when this subset is exposed to PM2.5.

In a clinical trial conducted with 80 individuals who were resident close to a coal-fired electric power plant in Brazil, biomarkers of oxidative status were utilized. It was demonstrated that a daily supplementation of 500 mg vitamin C and 800 mg vitamin E was protective against the effects of PM2.5 and restored the oxidative stress biomarkers to their normal levels (14).

Sadly, it now common for the levels of PM2.5 to exceed the level of 35 μg/m3 in the most polluted cities around the globe. The WHO say even these relatively modest levels lead to an increased mortality risk of 15%. It seems that nutrients with antioxidant and inflammatory properties such as fish oil, vitamins B, C and E and methyl nutrients are able to offer some protection against the physiological effects of PM2.5 exposure, though further work is required to better quantify this. It also likely that other nutrients with similar properties may have a beneficial effect.

1. Zhang W, Eggersdorfer, M., Salem N S, Chen, J J, Peter, S, & Qin, L.; “Nutrition Solutions to Counter Health Impact of Air Pollution : Scientific Evidence of Marine Omega-3 Fatty Acids and Vitamins Alleviating Some Harmful Effects of”; 2015;  2(2), 1–6. goo.gl/WH1TTY
2. Nutraceutical Business Review;  “Breathing Easy: Nutrient Solutions for Air Pollution”; 25th September 2014; goo.gl/g4dhdb
3. Montiel-Davalos A, Ibarra-Sanchez Mde. J, Ventura-Gallegos JL et al.; “Oxidative stress and apoptosis are induced in human endothelial cells exposed to urban particulate matter”; Toxicol In Vitro 2010; 24(1): 135-141.

4. Sun Q, Wang A, Jin X, et al., “ Long-term air pollution exposure and acceleration of atherosclerosis and vascular inflammation in an animal model”; J Am Med Assoc 2005;  294(23): 3003-3010.
5. Jedrychowski W, Masters E, Choi H et al. ; “Pre-pregnancy dietary vitamin A intake may alleviate the adverse birth outcomes associated with prenatal pollutant exposure: epidemiologic cohort study in Poland”; Int J Occup Environ Health. 2007; Apr-Jun;13(2):175-80.
6. Sram RJ, Binkova B, & Rossner P; “Vitamin C for DNA damage prevention”; Mutat Res. 2012 May 1;733(1-2):39-49. doi: 10.1016/j.mrfmmm.2011.12.001. Epub 2011 Dec 13.