Research increasingly points to environmental pollution as a contributor to osteoporosis: Recent studies describe a low-grade systemic inflammatory state that disrupts bone metabolism, shifting the balance toward increased bone resorption and decreased bone formation.

Two major risk factors stand out: exposure to heavy metals and inhalation of fine particulate matter (PM). Growing concern is prompting a re-evaluation of acceptable exposure levels and risk-reduction strategies. This was explained by Patrice Fardellone , a rheumatologist at the Amiens-Picardie University Hospital, Amiens, France, who presented at the 39th Annual Scientific Meeting of the Groupe de Recherche et d’Information sur les Ostéoporoses, Paris, on 16 January 2026.

Cadmium Reduces Bone Mineral Density (BMD)

Heavy metals share three main characteristics: high density (> 5 g/cm³), prolonged environmental persistence, and biological toxicity. They accumulate in organisms, sometimes at very low doses (bioaccumulation), and along food chains (biomagnification).

The heavy metals most frequently cited in the literature include lead, cadmium, arsenic, cobalt, and molybdenum, but also thallium and barium. A US study using the National Health and Nutrition Examination Survey database analyzed five cycles (2005-2006, 2007-2008, 2009-2010, 2013-2014, and 2017-2018) among 5745 adults of middle age. Heavy metal concentrations were measured in blood and urine, and 12 machine-learning models were applied to assess their association with BMD. Bone loss was defined as a T-score ≤ -1 compared with a “normal” group.

Among the heavy metals studied, cobalt, thorium, lead and, even more so, cadmium most frequently showed an association with lower BMD.

Cadmium is absorbed by inhalation and ingestion; inhalation comes mainly from tobacco — a single cigarette contains 0.1 µg-0.2 µg of cadmium — and from various industrial activities, including the production of nickel-cadmium batteries, dyes, thermal stabilizers for polyvinyl chloride and other plastics, anti-rust paints, fireworks, and fluorescent paints.

Cadmium ingestion is found in many foods, such as vegetables, fish, meats, offal, shellfish, and chocolate. The World Health Organization and the Food and Agriculture Organization define an acceptable daily intake of 60 µg-70 µg and a tolerable weekly intake of 0.4 mg-0.5 mg. “Cadmium exerts its Harmful effects on bone tissue by direct and indirect mechanisms,” Fardellone explained.

Regarding its direct action on bone cells, cadmium decreases osteogenesis. With respect to osteoblasts, it causes a drop in differentiation markers (Runx2, osteocalcin), extracellular matrix proteins (type I collagen), and bone alkaline phosphatases, as well as increased apoptosis, with cytoskeletal and DNA fragmentation.

Conversely, cadmium stimulates osteoclastogenesis, increasing both the number and activity of osteoclasts through elevations in parathyroid hormone and receptor activator of nuclear factor kappa B ligand, commonly known as RANKL. Indirectly, cadmium acts on the kidney to reduce synthesis of the active form of vitamin D, 1,25-dihydroxyvitamin D, also called calcitriol, with the expected consequences of increased urinary calcium loss and phosphaturia.

Recently, a PROSPERO-registered study (a marker of methodological quality) analyzed nearly 8000 women older than 50 years and assessed cadmium exposure: whether high or low, it was associated with a doubling of osteoporosis risk defined by densitometry (T-score ≤ -2.5 at any of the standard sites). For high exposure, the relative risk was 1.95 (95% CI, 1.39-2.73, P < .001); for low exposure, it was 1.99 (95% CI, 1.04-3.82; P = .040).

Airborne Particles Damage

Fine PM consists of solid or liquid particles suspended in the air with diameters < 10 µm. PM10 (diameter ≤ 10 µm) penetrates the upper airways, PM2.5 (diameter ≤ 2.5 µm) reaches the pulmonary alveoli, and ultrafine particles (PM0.1, diameter ≤ 0.1 µm) can enter the bloodstream.

These particles come from natural sources such as desert dust, sea spray, volcanoes, and pollen, but also from human activity, primarily vehicle emissions and wood heating, followed by industry (combustion), agriculture (ammonia) and smoking.

Particle size determines where they deposit in the respiratory tract: larger particles lead to respiratory complications such as asthma and bronchitis, whereas ultrafine particles that circulate in the blood can induce systemic inflammation, with potential repercussions for bone tissue.

On PMs, an Italian study conducted by the Italian Institute of Environment Protection and Research evaluated PM exposure in 59,950 women over nearly 4 years, from June 2016 to January 2020. Geographic distribution of PM2.5 concentrations, unsurprisingly, showed higher pollution around large urban areas and in industrial northern Italy compared with the more rural south. The analysis found that exposure to PM2.5 — but not to PM10 — was associated with a significant decrease in BMD at the femoral neck and lumbar spine.

Harmful Effects of Gaseous Pollutants

An analysis of 9041 women from the Women’s Health Initiative cohort (mean age, 63.3 ± 7.4 years) evaluated exposure to PM10 and gaseous pollutants (nitric oxide, nitrogen dioxide [NO₂], and sulfur dioxide [SO₂]) over the 1-, 3-, and 5-year periods preceding BMD measurement. Exposure to these pollutants over all periods considered was negatively correlated with BMD at all sites studied.

“This illustrates that beyond fine particles, other air pollutants are involved, such as SO₂, ozone, carbon monoxide (CO) and NO₂,” Fardellone said. “These compounds have shown adverse effects on bone tissue in several studies.”

Ozone in particular was implicated in a Taiwan study that combined two datasets: the Taiwan Biobank, which includes 4595 volunteers aged 30-70 years with no history of cancer, and the Taiwan Air Quality Monitoring Database, which gathers data from 74 pollutant‑monitoring stations.

The analysis showed that several pollutants were negatively correlated with BMD. PM2.5 and PM10 did not show a significant association with T-score, while ozone showed a positive association (unstandardized coefficient beta, 0.015; 95% CI, 0.004-0.026; P = .008).

CO (unstandardized coefficient beta, -0.809; 95% CI, -1.043 to -0.576; P < .001), SO₂ (unstandardized coefficient beta, -0.050; 95% CI, -0.085 to -0.015; P = .005), and NO₂ and other nitrogen oxides (NO_x) were negatively correlated with BMD (T-score).

In addition, “Synergies between certain pollutants have been identified,” Fardellone added. Interactions between NO_x and CO, and of NO₂ with SO₂, suggest their combined impact on BMD is multiplicative rather than merely additive.

Impact of Traffic-Related Pollution

A US Mexican study showed that proximity to a highway influences BMD. Among adults with a mean age of 34 years, those living within 500 m of a highway had lower BMD compared with those living more than 500 m away. The difference was 0.02 g/cm² for whole-body BMD and 0.03 g/cm² for pelvic BMD.

“These results suggest that traffic-related pollution could have a direct and proportional effect on the population’s bone mineral density,” Fardellone said.

PM Impact on BMD and Fractures

While that describes the association between PM and osteoporosis, a Korean study of more than 44,000 women older than 50 years evaluated the association between PM2.5 exposure and fracture risk.

Adjusted for age and the Charlson comorbidity index, the analysis shows a modest but significant effect of PM2.5 exposure on vertebral and peripheral fractures. The relative risk was 1.30 (95% CI, 1.02-1.24) for all fractures, 1.17 (95% CI, 1.00-1.38) for vertebral fractures, and 1.16 (95% CI, 1.01-1.33) for peripheral fractures.

Also addressing fractures, a US East Coast study analyzed 9.2 million Medicare beneficiaries aged 65 years or older from January 2003 to December 2010. Concentrations of black carbon — soot from incomplete combustion — were estimated with land-use-based spatiotemporal regression models, and higher black carbon levels were linked to greater loss of BMD over time.

Moreover, communities exposed to the highest annual PM2.5 concentrations had increased hospitalization rates for bone fractures. An increase of one IQR (4.18 µg/m³) in PM2.5 concentration corresponded to a 4.1% increase in the hospitalization rate for bone fractures.

Threat From Air and Chemical Pollution

In summary, recent work suggests that PM is an independent risk factor for low BMD and osteoporotic fractures.

Air pollutants affect bone tissue by two main mechanisms: induction of systemic inflammation and oxidative stress — several air pollutants can induce low-grade systemic inflammation that affects bone metabolism through cytokines such as TNF-alpha, interleukin-1-beta, interleukin-6, and interleukin-17 acting on osteoblast and osteoclast differentiation and function.

In addition, some pollutants, notably gaseous compounds, can cause oxidative damage in respiratory and bone cells. Different pollutant groups can also act as endocrine disruptors by binding to receptors on bone cells and altering their function. Air pollution may also lead, directly or indirectly, to vitamin D deficiency.

Characterizing these mechanisms will improve understanding of the pathophysiology of bone damage, and recognizing air pollution as a modifiable risk factor for osteoporosis could guide environmental policy.

This story was translated from Medscape’s French edition.