Traffic and Tobacco Add Pounds

Pollution—whether from tobacco smoke or car fumes—has been linked to obesity.

Researchers in Southern California asked recently whether children exposed to both would have higher rates of obesity. Crunching data on 3318 children enrolled in the Southern California Children’s Health Study, the researchers assessed road pollution exposure through traffic volume, proximity and meteorology. Tobacco exposure was included through parent questionnaire.

Results:

  • Maternal smoking during pregnancy was linked with BMI growth over 8-year follow-up
  • Second hand smoke exposure was associated with BMI growth
  • Compared to controls—children without exposure— children exposed to both high traffic pollution and second hand smoke increased BMI at a higher rate than either alone.

The authors concluded: “Our findings strengthen emerging evidence that exposure to tobacco smoke and NRP contribute to development of childhood obesity and suggest that combined exposures may have synergistic effects.”

Thus, the battle continues. Read more about the research here in Environmental Health Perspectives: A Longitudinal Cohort Study of Body Mass Index and Childhood Exposure to Secondhand Tobacco Smoke and Air Pollution: The Southern California Children’s Health Study.

Pollution Messes with Metabolism

Air pollution is not good for lungs. Just ask anyone in Beijing where surgical masks are a fashion accessory.

How bad is air pollution? The World Bank reported in 2010 that 16 of the world’s top 20 most polluted cities are in China. Linfen City in Shanxi Province, China, which is known for its coal industry, was the world’s most polluted.

Developed countries are polluted too.

Despite decades of cleanup measures, the American Lung Association State of the Air 2012 revealed that nearly half the population of the United States still suffers pollution levels that are often dangerous to breathe. The report found that unhealthy air posed a threat to the lives and health of more than 127 million people—roughly 41 percent of the nation. Even cities like Salt Lake City, Utah, and North Pole, Alaska, which sound pristine, are choking with pollution—the first from automobiles and industry and the latter from burning coal and wood for warmth. At times the air quality readings in North Pole are twice as bad as that of Beijing, according to Kim Murphy writing in the Los Angeles Times in 2013.

Air is judged by ozone and particulate matter. Greenhouse gases including carbon dioxide, methane, and nitrous oxide are bad for respiratory systems, according to the EPA. But a new slyer villain has emerged: the small bits, called particulate matter (PM).

According to the World Health Organization, PM affects more people than any other pollutant. 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.

And as you may have guessed by the recipe, these PM2.5s, which emerge from burning fuels, are linked to asthma, lung cancer and other respiratory diseases. People exposed to pollution don’t live as long. The mortality in cities with high levels of pollution exceeds that observed in relatively cleaner cities by 15 to 20 percent.

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.

In a new study published in Particle and Fibre Toxicology journal, special mice susceptible to Type 2 diabetes were exposed to either ambient PM2.5 or filtered air for 5 to 8 weeks.

Results:

  • O2, Co2, respiratory exchange and thermogenesis were all changed.
  • More insulin resistance
  • More visceral fat
  • More inflammation in spleen and visceral fat
  • Leptin levels increased
  • Gene expression in brown adipose tissue changed.

Air pollution may be adding to our obesity and diabetes numbers. Choking  on this epidemic is not an option.

 

 

 

Auto Pollution Fattens Future Generations

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.