Exposure to air pollution is associated with osteoporosis-related loss of bone mineral density and increased risk of bone fractures, according to a new study by researchers at Columbia University’s Mailman School of Public Health. Their findings, published in The Lancet Planetary Health reveal that:
- People living in areas of high air pollution are more likely to suffer bone fractures from osteoporosis:
- More people are hospitalized for osteoporosis fractures in areas with higher levels of air pollution;
- People exposed to car exhaust fumes have lower levels of a calcium-regulating hormone, leading to the brittle bone disease;
- Osteoporosis affects about 9 million people in the US, and the disease increases the risk of an early death by as much as 20 percent.
The study is the first to document higher rates of hospital admissions for bone fractures in communities with elevated levels of air pollution, showing increased risk of bone fracture admissions greatest in low-income communities. The research is based on a study of osteoporosis-related fracture hospital admissions among 9.2 million Medicare enrollees in the Northeast/Mid-Atlantic between 2003-2010.
The findings suggest that even a small increase in air pollution, especially the fine particles produced by fuel combustion in vehicles, power plants, and industrial manufacturing, lead to increases in bone fractures in older adults.
In a related, eight-year-long analysis of 692 middle-aged, low-income adults living in the Boston area, researchers found that those living in areas with higher levels of fine particulate matter and black carbon, another component of air pollution from automotive emissions, had reduced levels of parathyroid hormone, a key calcium and bone-related hormone, and experienced greater loses of bone mineral density than those exposed to lower levels of these pollutants.
Osteoporosis, the most common reason for a broken bone among the elderly, causes bones become to become brittle and weak as the body loses more bone mass than it can rebuild. There are an estimated 2 million osteoporosis-related bone fractures in the U.S. each year.
People with osteoporosis typically have no symptoms prior to a sudden fracture, which can happen spontaneously or from something as harmless as a hug.
In the year following a bone fracture an older adults risk for death increases by as much as 20 percent, and only 40 percent of those who experience fractures ever totally regain their independence.
Fine particulate matter air pollution is known to cause systemic oxidative damage and inflammation, which the researchers suggest could accelerate bone loss and increase risk of bone fractures in older individuals. Smoking, which contains several particulate matter components, has been consistently associated with bone damage.
“Decades of careful research has documented the health risks of air pollution, from cardiovascular and respiratory diseases, to cancer, and impaired cognition, and now osteoporosis,” says Andrea Baccarelli, MD, PhD, chair of Environmental Health Sciences at the Mailman School and the study’s senior author. “Among the many benefits of clean air, our research suggests, are improved bone health and a way to prevent bone fractures.”
In two studies published earlier this year, Baccarelli, a world leader in the science of epigenetics, reported that Vitamin B can diminish the effects of air pollution-induced cardiovascular disease, as well as epigenetic damage to DNA. It is unclear if the benefits of Vitamin B extend to bone loss. Even so, he says, the best way to prevent air-pollution-related diseases is through policies to improve air quality.
Source: Diddier Prada, Jia Zhong, Elena Colicino, Antonella Zanobetti, Joel Schwartz, Nicholas Dagincourt, Shona C Fang, Itai Kloog, Joseph M Zmuda, Michael Holick, Luis A Herrera, Lifang Hou, Francesca Dominici, Benedetta Bartali, Andrea A Baccarelli. Association of air particulate pollution with bone loss over time and bone fracture risk: analysis of data from two independent studies. The Lancet Planetary Health, 2017; 1 (8): e337 DOI: 10.1016/S2542-5196(17)30136-5