Adults, particularly those with a low income and aged at least 65 years, have an increased risk for bone fracture and osteoporosis-related loss of bone mineral density with long-term exposure to air pollution, according to findings published in The Lancet Planetary Health.
“In the United States, about 2.1 million osteoporosis-related bone fractures are reported each years, resulting in as much as $20.3 billion in annual direct health costs,” Andrea Baccarelli, MD, PhD, chair and Leon Hess professor of environmental health sciences at the Mailman School of Public Health, Columbia University, told Endocrine Today. “Not only that, but within 1 year of a bone fracture, the risk of death for older individuals increased by 10% to 20% with only 40% regaining full pre-fracture independence. When I started to study air pollution 10 years ago, all we knew was that it affected the lungs and the cardiovascular systems. Now we are realizing there is much more to it.”
Baccarelli and colleagues conducted two independent studies to determine the relationship between ambient concentrations of particulate matter and bone health.
In the first study, researchers evaluated data from 9.2 million Medicare enrollees aged at least 65 years from the Northeast/mid-Atlantic U.S. between 2003 and 2010 to determine the association of long-term concentrations of particulate matter less than 2.5 µm (PM2.5) and osteoporosis-related fracture hospital admissions.
Rates of bone fracture admissions were higher in communities with higher annual PM2.5 concentrations compared with lower concentrations, after controlling for covariates. The rate for hospital admission for bone fracture was 4.1% higher with each 1 interquartile range (IQR) increase in PM2.5 (RR = 1.041; 95% CI, 1.03-1.051).
In the second study, researchers evaluated data from the Boston Area Community Health/Bone Study (BACH/Bone Study) on 692 men (mean age, 46.7 years) with low-income to determine the association between long-term black carbon and PM2.5 concentrations with serum calcium homeostasis biomarkers and annualized BMD over 8 years.
Concentrations of parathyroid hormone were lower in participants living in locations with higher compared with lower concentrations of black carbon. Further, serum parathyroid concentrations were negatively associated with PM2.5 exposure.
BMD measures at baseline were not associated with PM2.5 or black carbon concentrations in participants’ residential areas. However, during the 8-year follow-up, participants living in areas with higher concentrations of ambient particles had higher loss of BMD at multiple anatomical sites. Femoral neck BMD decreased by 0.08% per year and ultradistal radius decreased by 0.06% per year with each 1 IQR increase in 1-year black carbon concentration at baseline.
“More research is needed to confirm these results on other populations to confirm that these results apply globally,” Baccarelli said. “All other effects of air pollution have been accepted as a fact after they have been found in multiple countries, for instance in the United States and Europe, where the population patterns differ. For instance, in the United States individuals with higher socioeconomic status often live in suburban areas that are less polluted while that is not true in Europe. While our results take into account socioeconomic factors, such as education, replication is necessary to fully exclude that the results are affected by concurrent population characteristics.”
In an accompanying editorial, Tuan V. Nguyen, PhD, principal research fellow and head of the genetics and epidemiology of osteoporosis lab, osteoporosis and bone biology division at Garvan Institute of Medical Research, St. Vincent’s Clinical School, University of New South Wales in Australia, wrote that, “Osteoporosis and its consequence of fragility fracture represent one of the most important public health problems worldwide because fracture is associated with increased mortality.
“It is now clear that genetic factors account for a modest proportion of fracture cases and bone density variance, suggesting that an environmental profile in the form of the exposure is likely the main driver of the disease,” he wrote. “Conceptually, an individual’s risk of fracture is grounded by the individual’s genome and modified by the individual’s exposome. The delineation of the interaction between genome and exposome has the potential to transform our thinking about the etiology of osteoporosis.” – by Amber Cox
For more information:
Andrea Baccarelli, MD, PhD, can be reached at firstname.lastname@example.org.
Disclosures: The authors report no relevant financial disclosures.