Diesel exhaust is a major donor to fine particles of air pollution, better known as PM 2.5. PMs are a jumble of solids, liquids, and organic and inorganic matter: mostly sulfate, nitrates, ammonia, sodium chloride, carbon, mineral dust, and water. The smaller ones at 2.5 µm are most dangerous because they easily invade the lungs.
Thick curtains of smog hanging over Asian cities tell of serious health implications for their residents. Indeed, exposure to PM2.5 heightens risk of heart disease and other inflammatory disorders, including obesity, research shows. According to the World Health Organization, PM affects more people than any other pollutant.
The unborn aren’t safe either. Pollutants can be powerfully toxic to growing fetuses, which don’t have these protective mechanisms of an adult: fully developed DNA repair tools, a capable immune system, detoxifying enzymes, complete liver metabolism, and a fully functional blood-brain barrier. Chemicals can pass through the placenta.
Also, the fetus has a fast metabolism, which can add to toxicity. When cells divide rapidly while being exposed to chemicals, things go wrong. And these changes, including tendency to obesity, may not appear until adulthood. Or even scarier, the damages may show up way down the road, in the cells of future generations. Genes are altered.
Look at what researchers at Virginia Commonwealth University in the United States found recently when they exposed pregnant female mice to PM 2.5: in addition to numerous injuries and oxidative stresses, the pups which had been exposed gained more weight by adulthood.
The link to obesity is new. How could this happen? The idea is that PM contributes to insulin resistance and adipose inflammation. In one experiment, mice exposed to PM2.5 showed insulin resistance and more visceral fat and inflammation among other defects.
Thus, the obesogenic effect of cars extends much beyond the toll exacted on exercise.