Breathing Bad Air May Boost Bone Fracture Risk

By | November 13, 2017

Two large studies link air pollution exposure to osteoporosis
by Salynn Boyles, Contributing Writer November 11, 2017

Action Points
• Poor air quality may be a modifiable risk factor for osteoporosis and bone fractures, especially among people living in low-income communities.
• Note that the studies are just the latest in a growing body of research linking air pollution exposure to osteoporosis.
Poor air quality may be a modifiable risk factor for osteoporosis and bone fractures, especially among people living in low-income communities, according to a newly published analysis of data from two independent studies.
In one study researchers documented higher rates of hospital admissions for bone fractures in communities exposed to elevated levels of ambient particulate matter (PM2.5) air pollution in an analysis of data on more than nine million Medicare enrollees.
In another 8-year follow-up of approximately 700 middle-age, low-income adults participating in a bone health study, participants living in areas with relatively high levels of PM2.5 and black carbon vehicle emissions had lower levels of a key calcium and bone-related hormone and greater decreases in bone mineral density than participants exposed to lower levels of these air pollutants.
All associations were linear and observed — at least for part of the PM2.5 distribution — at PM2.5 concentrations below the annual average limits set by the U.S. Environmental Protection Agency (12 μg/m3) and most other industrialized nations.
“Reducing emissions as a result of innovation in technologies or policy changes in emission standards of this modifiable risk factor might reduce the impact of air pollution on bone fracture and osteoporosis,” wrote Andrea Baccarelli, MD, PhD, chair of the Environmental Health Sciences Department and director of the Laboratory of Precision Environmental Biosciences at Columbia University’s Mailman School of Public Health in New York City, and colleagues, in Lancet Planetary Health.
In the hospital admission study, the team examined the association of long-term exposure to PM2.5 and hospital admissions for osteoporosis-related bone fractures among 9.2 million Medicare enrollees residing in the northeast, mid-Atlantic between January 2003 and December 2010.
In the second study, the researchers examined the association of long-term black carbon and PM2·5 concentrations with serum calcium homoeostasis biomarkers (parathyroid hormone, calcium, and 25-hydroxyvitamin [25(OH)D]) and annualized bone mineral density over 8 years (baseline, November 2002 — July 2005; follow-up, June 2010 — October 2012) of 692 middle-aged (46·7 years [SD12·3]), low-income men from the Boston Area Community Health/Bone Survey (BACH/Bone study) cohort.
PM2·5 concentrations were estimated using spatiotemporal hybrid modeling, including Aerosol Optical Depth data, spatial smoothing, and local predictors. Black carbon concentrations were estimated using spatiotemporal land-use regression models.
Among the main findings:
• In the Medicare analysis, risk of bone fracture admissions at osteoporosis-related sites was greater in areas with higher PM2·5 concentrations (risk ratio [RR] 1·041, 95% CI, 1·030 to 1·051; this risk was particularly high within low-income communities [RR 1·076, 95% CI, 1·052 to 1·100])
• In the longitudinal BACH/Bone study, baseline black carbon and PM2·5 concentrations were associated with lower serum parathyroid hormone (β=–1·16, 95% CI, –1·93 to –0·38, P=0·004, for 1 IQR increase [0·106 μg/m³] in the 1-year average of black carbon concentrations; β=–7·39, 95% CI, –14·17 to –0·61, P=0·03, for 1 IQR increase [2·18 μg/m³] in the 1-year average of PM2·5 concentrations)
• Black carbon concentration was associated with higher bone mineral density loss over time at multiple anatomical sites, including the femoral neck (–0·08% per year for 1 IQR increase, 95% CI, –0·14 to –0·02) and ultradistal radius (–0·06% per year for 1 IQR increase, –0·12 to –0·01)
• Black carbon and PM2·5 concentrations were not associated with serum calcium or serum 25(OH)D concentrations
The researchers acknowledged multiple limitations in both studies, which limit the ability to establish causality.
But in an editorial published with the studies, Tuan Nguyen, PhD, of the Garvan Institute of Medical Research in New South Wales, Australia, wrote that the studies are just the latest in a growing body of research linking air pollution exposure to osteoporosis: “Osteoporosis and its consequence of fragility fracture represent one of the most important public health problems worldwide because fracture is associated with increased mortality.”
He said 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 cumulative lifetime environmental exposures, known as exposome, is likely the main driver of disease.
“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.”

Funding for this research was provided by the National Institutes of Health, Institute on Aging, National Institute of Environmental Health Sciences, and the U.S. Environmental Protection Agency.
The researchers reported no relevant relationships with industry related to the study.
• Reviewed by Robert Jasmer, MD Associate Clinical Professor of Medicine, University of California, San Francisco and Dorothy Caputo, MA, BSN, RN, Nurse Planner
last updated 11.10.2017
• Primary Source
Lancet Planetary Health
Source Reference: Prada D, et al “Association of air particulate pollution with bone loss over time and bone fracture risk: analysis of data from two independent studies” Lancet Planetary Health 2017; DOI 10.1016/S2542-5196(17)30136-5.

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