The Skeleton as Environmental Portrait

How bone records pollution, stress, and the history of modern life

Bone Is Not a Passive Structure

Sandra Degen, a chemist with deep expertise in blood vessels, once told me something that reframed how I think about the body: blood vessels do far more than shuttle blood. They sense oxygen and nutrients, send signals that summon repairs, guide growth, and decide when—and where—healing should happen. They’re less like pipes and more like diplomats: listening, negotiating, coordinating.

Until recently, I carried a similar misconception about bone. Like most people, I thought of it as scaffolding—solid, durable, and largely inert.

But bones are neither quiet nor simple. They’re alive, fussy, and constantly remodeling. They store minerals and metals, respond to hormones, and stress, and continually rebuild themselves throughout life. They’re less like concrete pillars and more like coral reefs—busy, layered, and exquisitely sensitive to their surroundings.

How Common—and Costly—Bone Failure Really Is

Osteoporosis is far more common, and more dangerous, than most people realize. About one in three women and one in five men over age 50 will suffer a fracture because of it. For women, the toll is especially heavy: over a lifetime, they will spend more days hospitalized for osteoporosis than for breast cancer and heart disease combined.

Hip fractures are often the turning point. Within a year, one in four people will die. Of those who survive, many never walk independently again. These aren’t rare mishaps; they’re predictable failures of a system under long strain.

Osteoporosis is often framed as an inevitable disease of aging. But it emerged as a major public-health problem only in the second half of the twentieth century, when longer lives collided with industrialized environments and skeletons shaped by those conditions began to fail in large numbers.

What We Still Don’t Ask

Despite this burden, we rarely ask the most important question: why bones fail in the first place. Research has focused on repairs—drugs to slow bone loss, surgeries to replace joints—while paying far less attention to the forces that weaken the skeleton over decades.

Genes matter. Aging matters. Hormones matter. Early-life nutrition matters—especially when bones are first being built. But none of these tells the whole story. Bones are living tissues embedded in environments—and those environments have changed profoundly. If we want to understand why modern skeletons are struggling, we need to look beyond biology alone and toward the environmental triggers that quietly shape bone from the inside out.

Rickets: Our First Modern Bone Crisis

Christian Warren’s book, Starved for Light, reminds us that we’ve been here before. In the early twentieth century, rickets swept through industrial cities. Children raised in soot-darkened streets, deprived of sunlight and vitamin D, developed bowed legs, swollen joints, and brittle bones that fractured with ease. Their skulls softened. Their teeth weakened. Pelvises narrowed so severely that childbirth became dangerous, driving maternal mortality upward and fueling a boom market for forceps.

Bones are shaped by everything around them—sunlight, hormones, nutrients, pollution, stress, sleep, chemicals, and time. A skeleton is not merely a structure; it is an environmental portrait.

We curbed rickets with cleaner air and vitamin D fortification. But the lesson it taught was incomplete. Rickets and vitamin D deficiency did not cause the modern osteoporosis epidemic, but they likely helped prime it—lowering peak bone mass early in life and leaving skeletons less resilient decades later.

In that sense, rickets was not merely a childhood disease; it was an early warning. It showed how profoundly bone responds to environment—and how early those effects can be set. As overt deformities faded from view, subtler skeletal vulnerabilities remained, quietly carried forward into adulthood.

As the smoke thinned, a new and quieter suite of bone hazards crept in—chemicals invisible to the eye, but potent enough to alter the architecture of our internal scaffolding.

The Skeleton Is a Chemical Archive

Bone is not just scaffolding. It is the body’s mineral vault and metal archive. Roughly 95 percent of absorbed lead ends up stored in the skeleton, often sitting quietly for decades in cortical bone—the dense outer shell—only to be released during pregnancy, menopause, illness, or bone loss.

Lead doesn’t reinforce bone; it undermines it. Even tiny substitutions of lead for calcium can interfere with bone formation and strength. Because bone turns over slowly, those effects can linger—turning the skeleton into a long-term internal source of exposure.

Experimental studies show that lead weakens bone in ways density scans often miss. Rather than simply thinning bone, lead disrupts the cells that build and remodel it—impairing collagen formation and repair—so bones can appear adequately mineralized yet be structurally fragile. Even tiny substitutions of lead for calcium—well under one percent—can alter bone chemistry and reduce strength, producing a quiet loss of bone quality that accumulates as lead is stored in bone and released during periods of turnover.

Lead exposure also impairs balance, coordination, muscle strength, and reaction time. That matters because fractures are not only about weaker bones—they’re also about falling.

In a study of women, Khalil found that higher blood lead levels were associated with both increased non-vertebral fractures (such as the hip, wrist, and arm fractures) and more frequent falls. It’s not proof of cause and effect—but it is a troubling pairing. Small nudges toward weaker bone and poorer balance, acting together over time, can tip the scales toward fracture.

Fluoride offers a cautionary parallel. Promoters of fluoridation rarely reckon with this, but fluoride accumulates in bone, replacing hydroxyl groups in hydroxyapatite crystals. Yes, it increases density—and yes, that looks reassuring on a scan—but a randomized trial showed that fluoride-treated bones fracture more easily. They become chalk-hardened but brittle, like a seashell left too long in the sun.

Density is easy to measure. Strength is not.

Toxic Chemicals and the Skeleton

Newer studies raise a stranger possibility: synthetic chemicals may also infiltrate bone. They can provoke inflammation, confuse the cells that build and remodel bone, and subtly weaken structure as it is rebuilt.

Bone remodeling is a continuous construction project—old material removed here, new material laid down there, all according to a tightly regulated plan. Synthetic chemicals may act like contaminants on the job site: degrading materials, confusing signals, and weakening the structure as it is rebuilt.

The research is still young, but the clues are accumulating. And they echo a familiar pattern: tiny exposures, big consequences.

Forever Chemicals and Growing Bones

Research by Jessie Buckley and colleagues makes this life-course story concrete. In the HOME Study—a rare U.S. cohort followed from pregnancy into adolescence—higher PFAS exposure was associated with lower bone mineral content by age 12, especially cortical bone.

That distinction matters. Bone mineral content reflects how much bone is built; density reflects how tightly it’s packed. In growing children, content is often the better indicator of whether enough bone is being laid down during the brief window when peak bone mass is set.

Peak bone mass—roughly 40 to 60 percent of which is built during childhood and adolescence—sets the ceiling for skeletal health across the rest of life. Disruptions during this narrow window can translate into large differences in fracture risk decades later. When bone development is altered early, the damage may remain invisible for years, only surfacing later as fragility that looks like an inevitable consequence of aging, but isn’t.

Encouragingly, Buckley and her team also found that higher calcium intake, better overall diet quality, and moderate to vigorous physical activity attenuated some of the adverse associations between forever chemicals. Lifestyle interventions, it appears, may partially blunt the effects of exposures that have already occurred—but they do not erase them.

Taken together, these findings suggest something unsettling: bones may be recording the chemical signatures of modern life, carrying them forward for decades.

The Industrialization of Bone

Medicine treats joint replacements as routine maintenance—the orthopedic equivalent of changing a tire. But our ancestors walked more, lifted more, worked harder, and lived without ergonomic chairs or ibuprofen. And yet their joints often held up better.

The human skeleton as infrastructure—designed to last, shaped by how we live.

Archaeologists see this clearly. Preindustrial skeletons show wear and injury, but arthritis was generally milder and less common than today. Contrast that with modern life, where nearly one in three adults over 60 has had a knee or hip replacement. Somehow, a species that once built cathedrals and hauled firewood is now falling apart simply by living long enough to retire.

Why does the modern skeleton crumble?

Sedentary lives, chronic inflammation, nutritional gaps, and hormonal shifts all play roles. But environmental chemicals—quiet, constant, cumulative—may be a missing piece of the puzzle.

Imagine bone remodeling as a masonry crew rebuilding a stone wall. Now imagine someone sneaking in at night—swapping stones for brittle ones, dissolving mortar, scattering debris that disrupts the rhythm. The wall still stands, for a while. But its integrity is compromised.

That is what some chemicals may be doing to our bones.

Bones Are Telling Us Something

We curbed rickets once we understood that sunlight and vitamin D fortification mattered. Today we face a quieter crisis—less visible than bowed legs, but no less consequential—affecting millions of hips, knees, vertebrae, and shoulders. Yet research dollars still flow toward surgical fixes rather than environmental causes.

Bones keep bending, thinning, cracking, and collapsing under pressures we barely measure. And while orthopedic catalogs grow thicker each year, the fundamental question remains unanswered:

What, exactly, are we building our bodies out of?

Until we confront that question, bones will continue to whisper truths we’ve been reluctant to hear. And like rickets a century ago, they may be warning us—before the rest of the body breaks.