Other environmental factors and the risk of type 1 diabetes

Yes, national registries in Europe, North America, and Asia consistently show more new cases of type 1 diabetes diagnosed in autumn and winter compared with the summer months. The pattern is more pronounced in school-age children and adolescents, and in young adults, although it remains visible, it is clearly more attenuated. Viruses that can penetrate the pancreatic beta cells, such as enteroviruses (especially Coxsackie B), influenza viruses, and respiratory syncytial virus, circulate more intensely in winter. They could trigger or accelerate the autoimmune process in genetically predisposed people [1].

In parallel, exposure to ultraviolet radiation drops dramatically in winter (especially north of the 37th parallel, and therefore across most of Europe). As a result, there is a significant fall in the cutaneous synthesis of vitamin D, a nutrient and hormone with an immunomodulatory role. Cold increases metabolic demand, the need for insulin, and, consequently, the strain on already-affected beta cells, possibly hastening the onset of clinical symptoms. Seasonal variation is also linked to latitude. At northern latitudes the seasonal oscillation of diagnoses is more pronounced, while close to the equator the effect attenuates. Seasonality suggests that a mix of factors (infections, sunlight, metabolic stress) acts as triggers, but no season alone can cause the disease [2].

The main pollutants studied are:

• fine particles (PM2.5);
• coarse particles (PM10);
• nitrogen dioxide (NO₂);
• ozone (O₃);
• sulfur dioxide;
• heavy metals associated with road traffic and industrial activities.

The biological mechanisms by which these pollutants may influence autoimmune risk are plausible and documented at the experimental level. Inhaled particles activate immune cells in the lung, thereby triggering systemic inflammation through the release of pro-inflammatory cytokines (chemical signals that sustain inflammation). In addition, pollutants can disrupt the balance of T-lymphocyte subsets (the white blood cells that coordinate immune defense) and reduce the function of regulatory T cells (the ones that keep immune reactions in check), weakening immune tolerance [3].

Prenatal exposure is particularly important, because the development of the fetal pancreas and the programming of the immune system take place in the womb. Early childhood is another window of vulnerability. It is useful to view air pollution as a possible contributor, not as a direct cause. You can monitor the air quality index in your city. Reduce outdoor activity when PM2.5 or ozone levels are high. Avoid active and passive smoking, especially during pregnancy and around children [4].

Pesticides and other persistent chemicals are being investigated as possible modulators of type 1 diabetes risk, particularly through their effects on the pancreatic beta cells and on the immune system. Relevant categories include:

• organophosphate pesticides and carbamates — currently used in agriculture;
• organochlorine pesticides (such as DDT and its metabolites, hexachlorobenzene, certain PCBs, that is, polychlorinated biphenyls) — although banned in many countries, they persist in the soil, the food chain, and human adipose tissue;
• pyrethroids.

Occupational exposure produces the largest accumulations, but for most people the main exposure is dietary (residues on fruit, vegetables, fish, milk, meat) and from the home [5].

The proposed mechanisms include direct toxicity to beta cells with induction of apoptosis (programmed cell death), alteration of the gut microbiota, and activation of receptors that amplify oxidative stress. Wash fruit and vegetables well under running water and remove the outer leaves of leafy vegetables. Diversify your food sources and consider organic products for food categories prone to higher residues, such as strawberries, spinach, or grapes. Pregnant women and families involved in farming should use protective equipment. Type 1 diabetes does not arise from a single chemical, but in the context of a genetic vulnerability over which several environmental factors are layered [6].

Yes, at the population level. On a global scale, the incidence of type 1 diabetes is generally higher in heavily urbanized and industrialized countries and lower in regions with a low level of development. Some children from low-incidence regions move to high-incidence regions, and migration studies show that their risk approaches that of the new environment. This indicates a clearly more important role for environmental factors, which comes on top of genetic susceptibility. Urbanization brings a whole package of harmful exposures that converge on the immune system:

• air pollution;
• a diet rich in ultra-processed foods and low in fiber;
• a sedentary lifestyle;
• chronic psychosocial stress;
• smaller family sizes;
• more frequent caesarean births;
• wider use of antibiotics in the first years of life;
• reduced exposure to the microbial diversity of soil, plants, and animals [2].

It is not "rurality" itself that protects, but certain specific exposures, such as contact with animals, biodiversity, or unprocessed food. If you live in a city, try to spend as much time as possible each week in the green spaces you have within reach. Give children the opportunity to have contact with nature and, if possible, with pets. Take physical activity outdoors and use antibiotics only when truly necessary. A diet rich in vegetables, whole grains, fish, and fermented foods supports a diverse gut microbiome. These choices do not prevent type 1 diabetes. They do counterbalance some of the pro-inflammatory pressures of urban life that, in combination with genetic predisposition, may favor the onset of the disease [7].

Type 1 diabetes has one of the most marked geographic gradients of any chronic disease. Incidence tends to increase as you move further from the equator. Countries such as Finland, Sweden, Norway, Denmark, the United Kingdom, and Canada have high rates, while equatorial regions in sub-Saharan Africa, South Asia, and Latin America report lower values, although these are constantly rising along with urbanization. Sardinia is an exception. Although it is located closer to the equator (the Mediterranean), it has an incidence comparable to that of the Nordic countries [8].

The proposed mechanisms for the latitudinal gradient involve:

• reduced exposure to ultraviolet B radiation at northern latitudes, with lower cutaneous synthesis of vitamin D;
• lower temperatures (which alter viral transmission);
• prolonged time spent indoors in winter;
• circadian rhythms disrupted by days that are too short or too long.

Latitude should be viewed as a proxy (an indirect indicator) for a set of exposures. The practical message is to maintain an adequate vitamin D level throughout the year, especially in winter or if you live at northern latitudes. Latitude does influence risk, but no climate on its own causes the disease and no climate absolutely protects you from type 1 diabetes [9].

Drinking water quality has been investigated for decades as a possible contributor to type 1 diabetes risk. The reason is that the global incidence is rising faster than genetic changes can explain. Nitrates and nitrites from agricultural fertilizers and livestock waste contaminate groundwater. Their metabolic conversion into N-nitroso compounds (substances formed in the body from nitrates and nitrites), with cytotoxic potential on beta cells, offers a plausible biological hypothesis. The internationally recommended limit is approximately 50 mg/L for nitrate in drinking water (the WHO standard). Infants and young children are most susceptible. Heavy metals such as arsenic and lead, present in groundwater or released from old plumbing, can interfere with insulin signalling and immune balance [10].

There is also a reverse hypothesis, related to hygiene (the hygiene hypothesis). Highly chlorinated municipal water and other sanitary protection behaviors reduce a child's early exposure to environmental micro-organisms. Through this lack of training, the immune system could mature more slowly. The threshold of tolerance to beta cell antigens falls, and exposure to various triggers later on can more easily initiate the autoimmune process. If you use a private source (a well), test the water periodically for nitrates and heavy metals, especially near agricultural or industrial areas. Reverse osmosis filters, ion exchangers, or distillation remove nitrates. Carbon filters do not. Clean drinking water is a fundamental public health issue. Its specific contribution to type 1 diabetes risk remains modest, however, within a multifactorial landscape dominated by genetics, infections, microbiome, and nutrition [7].

Endocrine disruptors are natural or synthetic chemical substances that mimic, block, or interfere with the body's hormones. The best known are:

• the bisphenols (BPA, BPS, BPF);
• phthalates (used in soft PVC, food packaging, scented cosmetics, vinyl toys);
• persistent organic pollutants;
• dioxins;
• certain pesticides;
• perfluorinated compounds (PFAS).

Typical daily sources include:

• the inner lining of cans;
• polycarbonate plastics;
• thermal paper receipts;
• flexible food packaging;
• plastic films;
• perfumes;
• nail polishes;
• cosmetic products not labeled "phthalate-free".

These substances migrate more easily into food and drink in the presence of heat, fat, and acidity. BPA can alter insulin secretion and induce oxidative stress in the beta cells. Endocrine disruptors modulate the balance of T-lymphocyte subsets, disrupt the function of regulatory T cells, alter the gut microbiome, and can epigenetically reprogram some genes involved in immune tolerance, that is, they can change the activity of those genes without altering the genetic code [11].

The perinatal window is particularly important. Endocrine disruptors cross the placenta, are present in breast milk, and the doses received involuntarily per kilogram of body weight are higher in infants than in adults. Preferentially choose fresh or frozen foods over canned and ultra-processed products. Store and heat food in glass, ceramic, or stainless steel containers. Never put plastic in the microwave. Decline thermal paper receipts when you do not need them and wash your hands after touching them. These choices reduce overall chemical exposure, without being specific prevention measures for type 1 diabetes, which remains a disease of multifactorial origin [6].

Microplastics are plastic particles smaller than 5 mm, and nanoplastics are smaller than 1 micrometer. They appear through the fragmentation of larger plastics and through direct shedding from packaging, bottles, synthetic textiles, tyres, and cosmetic products. Daily sources of exposure include:

• water bottled in plastic, especially when heated or reused;
• food films;
• "take-away" containers;
• baby bottles sterilized at high temperatures;
• tea bags with plastic fibers;
• plastic chopping boards;
• indoor dust;
• even tap water.

Heating food in plastic containers in the microwave releases significant amounts of microplastics and nanoplastics [12].

The proposed mechanisms for possible involvement in type 1 diabetes are still theoretical and come from animal models. They could include:

• disruption of the intestinal barrier ("leaky gut") and dysbiosis, that is, an imbalance of the gut flora;
• activation of macrophages with a pro-inflammatory profile;
• transport and release in the gut of substances adsorbed onto the surface of plastics (BPA, phthalates, persistent organic pollutants, heavy metals);
• oxidative stress in the immune system and the pancreatic beta cells.

The recommendations for you are precautionary. Never heat food in plastic, not even in containers labeled "microwave-safe". Use reusable stainless steel or glass bottles instead of single-use plastic ones. Avoid storing acidic foods, such as tomato sauces or citrus, in plastic containers. Remember that the "BPA-free" label does not guarantee safety, since substitutes such as BPS and BPF have similar effects [6].