While inflammation rages in your fat tissue, pollution triggers a second attack. This is oxidative stress.
Published Nov 19, 2025 | 7:00 AM ⚊ Updated Nov 19, 2025 | 7:00 AM
Representational image. Credit: iStock
Synopsis: At the RSSDI diabetes conference in Kerala, doctors warned that breathing polluted air is helping fuel India’s diabetes explosion. Tiny particles (PM2.5) get deep into the lungs, cause long-term inflammation, confuse the body’s insulin system, and make blood sugar control harder. Even a small rise in pollution levels sharply increases the risk of diabetes, especially for kids and the elderly.
Picture this: You step outside for your morning walk. The air hangs thick and grey. You take a breath, and invisible particles, 30 times smaller than a strand of hair rush into your lungs.
Within minutes, these particles trigger a chain reaction in your body that, over months and years, can make your cells stop responding to insulin. Your risk of diabetes climbs with every breath.
This is not science fiction. This is happening across majority of India’s cities today.
At the 53rd National Conference of the Research Society for the Study of Diabetes in India (RSSDI) held in Kerala this week, experts presented evidence that environmental pollution has emerged as a major driver of the country’s diabetes epidemic.
Dr Vitull K. Gupta, Chairman of the Association of Physicians of India (Malwa Branch), called environmental pollutants and endocrine disruptors “a new frontier in diabetology,” demanding attention to “the interplay of industrialisation, environmental exposures, and metabolic health.”
Dr Ajoy Tewari, Secretary of RSSDI, shared research on residents exposed to poor air quality. Air quality levels between 180 and 220 micrograms per cubic metre are common across many Indian cities.
Such exposure could increase insulin resistance by 72 percent to 90 percent. Insulin resistance means your body’s cells start ignoring insulin’s signal to absorb sugar. It’s like a door that stops responding when you turn the key. This is the first step toward diabetes.
“These figures are concerning,” Professor Narsingh Verma, Chairman of RSSDI, said.
“Pollution has transcended environmental boundaries, posing a serious threat to metabolic health and heightening diabetes risk, particularly among vulnerable groups such as children, the elderly, and those predisposed to the condition.”
A systematic review and meta-analysis titled “Long-term exposure to air pollution and risk of insulin resistance” revealed something remarkable: for every single microgram per cubic metre increase in PM2.5, your HOMA-IR rises by 0.40 percent. HOMA-IR measures how resistant your cells are to insulin. Cleaner air directly translates to better blood sugar control.
But how does breathing polluted air make your blood sugar rise? The answer lies in three biological pathways. These pathways transform your lungs into a gateway for metabolic disease.
When you inhale polluted air, particles called PM2.5 travel deep into your lungs. PM2.5 stands for particulate matter measuring 2.5 micrometres. To understand how small these are, take a grain of beach sand. Imagine dividing it into 25 pieces. Each piece would still be larger than PM2.5. These particles are incredibly tiny. They slip past your nasal hair and throat. They even sneak into the branching tubes of your airways and travel all the way down to where oxygen enters your blood.
They land in the alveoli. These are millions of tiny balloon-like sacs where your lungs and blood meet. Each alveolus is wrapped in blood vessels thinner than thread. When PM2.5 settles here, guardian cells detect the invasion. These cells are called alveolar macrophages and bronchial epithelial cells. Think of them as security guards patrolling your lung tissue.
These cells release chemical alarm signals. The signals are tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β). Scientists call these proinflammatory cytokines. You can think of them as emergency sirens that your lung cells blast.
“Discussions about pollution frequently focus on its respiratory implications, but we often overlook its influence on blood glucose levels,” Dr Tewari said. “Air quality is evolving into a metabolic hazard.”
These alarm signals pour into your bloodstream. They flood through your body like messages in a group chat. Your body switches into defence mode.
It activates inflammation throughout your system. But unlike a cut that heals or a cold that passes, pollution exposure continues. Day after day, your body stays inflamed. Month after month, this creates chronic low-grade inflammation. It’s like having a fire alarm that never stops ringing.
The inflammatory signals travel through your blood vessels. They reach visceral adipose tissue. This is the fat packed around your internal organs, the kind that gives you a belly. Here, something remarkable happens. The alarm signals call white blood cells called monocytes out of your bloodstream. These cells migrate into your fat tissue.
Studies using specially marked mice showed a sixfold increase in these immune cells. They migrated into belly fat after pollution exposure. Imagine your fat tissue as a peaceful neighbourhood. Suddenly it sees six times more police cars patrolling its streets. The reason? Constant alarm calls.
Once inside, these monocytes transform into macrophages. These cells normally eat bacteria and debris. But in this inflamed state, they shift into attack mode. They pump out more TNF-α and IL-6. They reduce IL-10, an anti-inflammatory signal. It’s like neighbourhood watch volunteers who become paranoid. They start causing problems instead of preventing them.
These activated macrophages disrupt how fat cells communicate with insulin. They trigger lipolysis. That’s the breakdown of stored fat. This floods your bloodstream with free fatty acids. These fatty acids are like oil spilled on a road. They make everything slippery. They prevent insulin from doing its job of guiding sugar into cells.
At the conference, a researcher from Lucknow’s Wellness Clinic presented related findings. Smita Singh showed that 58 percent of women with type 2 diabetes were emotional eaters. Only 34 percent of men showed this pattern. “Interpersonal partner violence is an emerging determinant influencing maladaptive eating and poor metabolic outcomes,” she said, highlighting how stress compounds the biological damage from pollution.
While inflammation rages in your fat tissue, pollution triggers a second attack. This is oxidative stress. Pollutants generate reactive oxygen species. Scientists call these unstable molecules free radicals. Think of free radicals as rust spreading through metal. Except this rust damages the machinery inside your cells.
These molecules activate an enzyme called NADPH oxidase. This enzyme produces even more free radicals. It’s a vicious cycle. It’s like a small fire that starts generating its own fuel. Studies proved this connection by testing special mice. These mice lacked a component called p47phox. This component helps make NADPH oxidase work. These mice remained protected from pollution-induced insulin resistance. This confirmed that free radicals drive the damage.
The free radicals attack insulin receptors on your cell surfaces. These are the molecular locks that recognize insulin’s key. When rust corrodes a lock, the key stops working. Similarly, damaged insulin receptors stop responding to insulin. The free radicals also sabotage GLUT-4. This is a protein that acts like a doorway letting glucose enter cells. With broken locks and jammed doors, sugar accumulates in your blood. It cannot enter cells that need it.
In your liver—the body’s sugar warehouse—pollution exposure disrupts the chemical chain reaction. This reaction normally responds to insulin. Specifically, it reduces tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1). It also decreases Akt phosphorylation. These are steps in insulin’s messaging system. Think of them like relay runners passing a baton. When pollution disrupts these handoffs, the message “store this sugar” never arrives.
The third pathway involves your cells’ protein factories. These structures are called the endoplasmic reticulum, or ER. Inside every cell, the ER folds newly made proteins into precise shapes. It’s like origami. Each protein must fold correctly to function. The ER has quality control inspectors that check every protein.
Pollutants overwhelm this system. Misfolded proteins pile up like defective products jamming an assembly line. This triggers ER stress. It activates emergency pathways called ATF6 and PERK-eIF2α signalling. These pathways induce stress-related proteins such as CHOP/GADD153. Ironically, these proteins make the problem worse. They impair the cell’s ability to respond to insulin and process glucose.
In your liver, prolonged ER stress creates a serious condition. It resembles nonalcoholic steatohepatitis (NASH). Essentially, it’s a fatty, inflamed liver even if you never drink alcohol. Fat accumulates in liver cells. The liver loses its ability to store sugar as glycogen. It cannot release sugar when needed. Your body’s glucose thermostat breaks.
“Indians are particularly vulnerable due to a combination of low protein intake, frequent consumption of fried carbohydrates, and worsening air pollution,” Peter Schwarz, President of the International Diabetes Federation, told the conference. “Even slim individuals in India are prone to fatty liver because of these dietary patterns.”
When you fry carbohydrates, the high heat changes their molecular structure. Think of that crispy dosa or those golden pakoras. They become harder for your liver to process. Add pollution-induced ER stress. Your liver faces a perfect storm.
Beyond these three main pathways, PM2.5 attacks your blood vessels. The endothelium lines every blood vessel in your body. It’s a single layer of cells. It acts like smooth tiles allowing blood to flow freely. Pollution particles damage this lining. They make it rough and dysfunctional.
Damaged blood vessels struggle to regulate blood flow. This means glucose has trouble reaching tissues that need it. It’s like having traffic jams on the highways that deliver supplies.
Particulate matter also carries hitchhikers. These are lipopolysaccharides (LPS) and oxidised phospholipids. They’re bacterial fragments and damaged fats. These activate Toll-like receptor 4 (TLR4) and the NLRP3 inflammasome. These are alarm systems normally reserved for detecting infections. Research shows that LPS-binding protein levels correlate with diabetes risk. This means pollution tricks your immune system. It thinks you have a chronic infection.
These activated alarm systems trigger NF-κB and JNK signalling pathways. These pathways block insulin action. Your body’s defence mechanisms accidentally sabotage your metabolism while fighting pollution.
Dr Gupta highlighted another environmental threat discussed at the conference. This threat is phthalates. These are chemicals used to make plastics flexible. They leach from plastic food containers, water bottles, and packaging. Indian research indicates phthalates epigenetically increase type 2 diabetes risk. This means they change how your genes express without altering the genes themselves. It’s like changing the volume on a stereo without rewiring it.
“Environmental pollutants and endocrine disruptors represent a new frontier in diabetology,” Dr Gupta said, noting these chemicals pose particular hazards to pregnant women by altering gene expression related to insulin sensitivity in developing babies.
(Edited by Amit Vasudev)
