Smoking is the single biggest risk factor for emphysema, but it’s far from the only one. Age, genetics, workplace exposures, air pollution, certain infections, and even secondhand smoke all play a role in whether the tiny air sacs in your lungs break down over time. Understanding these risk factors matters because some are avoidable, and catching the modifiable ones early can slow or prevent damage.
Cigarette Smoking
Smoking causes the vast majority of emphysema cases. The damage happens because cigarette smoke triggers an ongoing inflammatory response deep in the lungs, breaking down the walls of the air sacs (alveoli) that exchange oxygen and carbon dioxide. Over years, this destruction leaves fewer, larger, less efficient air sacs, and the damage is permanent.
The risk scales sharply with how much and how long you smoke. A long-term study tracking people from young adulthood into middle age found that heavy, steady smokers had roughly 26 times the odds of developing emphysema compared to people who never smoked. But even light smoking is dangerous. People who smoked at a low rate over many years had about 8 times the odds of emphysema versus nonsmokers, partly because low-rate smokers tend to inhale more deeply or take more puffs per cigarette, pulling smoke further into the lungs.
One encouraging finding: quitting matters at any level. Low-rate smokers who quit had lower emphysema odds than those who kept smoking, even when the quitters had accumulated more total cigarette exposure over their lifetimes. The lungs can’t fully repair emphysema damage that’s already occurred, but stopping smoking halts the progression.
Secondhand Smoke
You don’t have to smoke yourself. Long-term exposure to other people’s cigarette smoke independently raises your risk of developing COPD, which includes emphysema. People regularly exposed to secondhand smoke have about a 49% higher risk of developing COPD compared to those with no exposure, after adjusting for other factors.
The relationship follows a dose-response pattern, meaning more hours of exposure equals more risk. Each additional hour of secondhand smoke per week increases the likelihood of COPD by about 3%. People exposed to more than 5 hours of secondhand smoke per day face roughly 1.5 times the risk of being diagnosed with chronic bronchitis or emphysema. Even moderate exposure of 20 or more hours per week is enough to measurably raise COPD risk.
Age and Natural Lung Changes
Emphysema is most commonly diagnosed in people over 50, and aging itself sets the stage for the disease. As you get older, your lung tissue gradually loses elasticity and your air sacs naturally enlarge. Between ages 50 and 70, the average diameter of an alveolus increases from about 265 to 453 micrometers. In someone with emphysema on top of aging, those air sacs stretch even further, to around 530 micrometers.
Aging also weakens the lung’s ability to repair itself. Cells become senescent, meaning they stop dividing and functioning normally. This makes older lung tissue less tolerant of damage from smoke, pollution, or other insults. Research in animal models confirms this: older mice exposed to the same irritants as younger mice developed emphysema significantly faster. The relationship works both ways, too. Emphysema appears to accelerate the aging process in lung cells, creating a cycle where the disease and aging reinforce each other. This helps explain why COPD tends to progress faster in older patients.
Alpha-1 Antitrypsin Deficiency
The most well-established genetic risk factor for emphysema is a condition called alpha-1 antitrypsin deficiency (AATD). Your liver produces a protein that travels to your lungs and protects them from an enzyme called neutrophil elastase, which is released by immune cells and can chew through lung tissue. When your body doesn’t produce enough of this protective protein, that enzyme goes unchecked and gradually destroys the air sacs.
AATD affects roughly 1 in every 3,000 to 5,000 people in North America, making it about as common as cystic fibrosis. Up to 5% of people diagnosed with COPD are thought to have this deficiency, yet only about 4 to 5% of those who carry it have actually been identified. People with AATD often develop emphysema at a younger age, sometimes in their 30s or 40s, especially if they also smoke. If you’re diagnosed with emphysema unusually early or have a family history of lung disease, testing for this deficiency is straightforward with a blood test.
Workplace Dust and Fumes
Occupational exposures account for a meaningful share of emphysema cases, particularly among people who work in mining, construction, manufacturing, or agriculture. Inorganic dust, which includes particles from silica, coal, and cadmium, has the strongest and most consistent link to emphysema. Studies of coal miners, gold miners, and workers exposed to cadmium dust have repeatedly shown elevated rates of the disease.
Fumes from combustion processes also pose a risk. These produce extremely fine particles that can travel deep into the smallest airways and reach the alveoli, where gas exchange happens. A large Swedish study found that workers exposed to inorganic dust had 21 to 37% higher odds of emphysema, and the association held up even after accounting for smoking. For people who both smoke and face workplace exposures, the risks compound.
Indoor and Outdoor Air Pollution
For billions of people worldwide, the most relevant risk factor isn’t cigarettes but the air inside their own homes. Biomass fuels like wood, charcoal, crop waste, and animal dung are used for cooking and heating by much of the world’s population, and burning them releases carbon monoxide, fine particulate matter, benzene, and other toxic compounds. Particulate matter levels inside homes burning biomass fuels can be 10 to 70 times higher than outdoor ambient levels, and carbon monoxide during cooking can reach 500 parts per million, far beyond safe thresholds.
Because cooking is the primary source of this exposure, women and children bear the greatest burden. In developing countries, girls often begin cooking around age 15 and spend 4 to 6 hours daily in poorly ventilated kitchens. Over 90% of COPD-related deaths occur in low- and middle-income countries, where biomass smoke exposure is widespread. In these regions, indoor air pollution accounts for a significant proportion of COPD cases, compared to high-income countries where tobacco smoking drives over 70% of cases.
Outdoor air pollution matters too, particularly fine particulate matter known as PM2.5. Research comparing urban and rural populations has shown that higher ambient PM2.5 concentrations correlate with higher COPD rates. Animal studies demonstrate that long-term PM2.5 exposure causes measurable airspace enlargement and lung function decline consistent with emphysema. PM2.5 particles are small enough to penetrate deep into the lungs, where they trigger chronic inflammation that gradually damages tissue.
HIV Infection
HIV is an independent risk factor for emphysema, separate from the higher smoking rates seen among people living with HIV. In one study comparing people with and without HIV who had similar smoking histories, 33% of those with HIV had significant emphysema on CT scans, compared to only 17% of those without HIV. After adjusting for smoking, HIV infection more than doubled the odds of emphysema.
The likely explanation involves chronic immune activation. HIV keeps the immune system in a persistent state of inflammation, and markers of this activation correlate with emphysema severity. People living with HIV who have experienced significant drops in their immune cell counts appear to be at the highest risk, suggesting that immune damage plays a direct role in lung tissue breakdown.
E-Cigarettes and Vaping
Evidence is still building, but the data so far is not reassuring. A meta-analysis of available studies found that current e-cigarette users had 48% higher odds of having COPD compared to non-users, while former e-cigarette users had 84% higher odds. E-cigarette aerosols contain formaldehyde, acrolein, acetaldehyde, ultrafine particles, and reactive oxygen species, all of which can cause airway inflammation, oxidative stress, and tissue damage similar to the effects of traditional cigarette smoke.
Some researchers argue the evidence so far only shows mild, short-term respiratory irritation and doesn’t prove vaping causes serious lung disease. The challenge is that e-cigarettes haven’t been around long enough to study the kind of decades-long exposure that produces emphysema from traditional smoking. Given the known presence of lung-damaging chemicals in the aerosol, the risk is plausible and the early data points in a concerning direction.
Asthma and Airway Sensitivity
People with asthma or heightened airway reactivity face a higher risk of eventually developing COPD, including emphysema. A large retrospective study following over 9,600 people for 11 years found that those with increased airway responsiveness, where the airways overreact and narrow in response to triggers, had a higher incidence of COPD. Chronic, poorly controlled asthma can cause permanent structural changes in the airways over time, a process called airway remodeling, that overlaps with the changes seen in COPD. This has led to the recognition of an asthma-COPD overlap, where features of both conditions coexist in the same patient.