📘 Other environmental factors and the risk of type 1 diabetes

Yes, national registries from Europe, North America, and Asia consistently show more new cases of T1D 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 pancreatic beta cells, such as enteroviruses (especially Coxsackie B), influenza viruses, and respiratory syncytial virus circulate more intensely in winter and could trigger or accelerate the autoimmune process in genetically predisposed individuals [2].

In parallel, exposure to ultraviolet radiation drops dramatically in winter (especially above the 37th parallel), which significantly reduces the cutaneous synthesis of vitamin D, a nutrient and hormone with an immunomodulatory role. Cold increases metabolic demand and 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 [1].

The main pollutants studied are fine particles (PM2.5), coarse particles (PM10), nitrogen dioxide (NO₂), ozone (O₃), and sulfur dioxide, as well as 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. In addition, pollutants can disrupt the balance of T-lymphocyte subsets and reduce the function of regulatory T cells, 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. The only thing you can do is monitor the air quality index in your city and 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 T1D risk, particularly through their effects on 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), which, although banned in many countries, persist in the soil, the food chain, and human adipose tissue, as well as pyrethroids. Occupational exposure produces the largest accumulations, but for most people, the main exposure is dietary (residues on fruits, vegetables, fish, milk, meat) and from the home [5].

The proposed mechanisms include direct toxicity to beta cells with induction of apoptosis, alteration of the gut microbiota, and activation of receptors that amplify oxidative stress. Wash fruits and vegetables well under running water and remove the outer leaves of leafy vegetables. Diversify 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. T1D does not arise from a single chemical, but in the context of genetic vulnerability over which several environmental factors are layered [6].

On a global scale, the incidence of T1D is generally higher in heavily urbanized and industrialized countries and lower in regions with a low level of development. Migration studies show that when children from low-incidence regions move to high-incidence regions, their risk approaches that of the new environment, indicating a clearly more important role of environmental factors that comes on top of genetic susceptibility. Urbanization brings a whole package of harmful exposures that converge on the immune system, such as 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, and reduced exposure to microbial diversity from soil, plants, and animals [1].

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 weekly in the green spaces you have available, give children the opportunity to have contact with nature and, if possible, with pets, do physical activity outdoors, and use antibiotics only when truly necessary. A diet rich in vegetables, whole grains, fish, and fermented sources supports a diverse gut microbiome. These choices do not prevent T1D, but they counterbalance some of the pro-inflammatory pressures of urban life that, in combination with genetic predisposition, may favor the onset of the disease [7].

T1D 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 [9].

The proposed mechanisms for the latitudinal gradient involve reduced exposure to ultraviolet B radiation at northern latitudes, with lower cutaneous synthesis of vitamin D. To this is added lower temperature (which alters viral transmission), prolonged time spent indoors in winter, and circadian rhythms disrupted by days that are too short or too long. Latitude should be viewed as a proxy for a set of exposures. The practical message is to maintain an adequate vitamin D status throughout the year, especially in winter or if you live at northern latitudes. No climate puts you at risk and no climate absolutely protects you from T1D [8].

Drinking water quality has been investigated for decades as a possible contributor to T1D risk, especially because the global incidence is rising faster than can be explained by genetic changes. Nitrates and nitrites from agricultural fertilizers and livestock waste contaminate groundwater, and their metabolic conversion into N-nitroso compounds, with cytotoxic potential on beta cells, offers a plausible biological hypothesis. The internationally recommended limits are approximately 50 mg/L for nitrate in drinking water (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 signaling and immune balance [10].

There is also a reverse hypothesis, related to hygiene (the hygiene hypothesis), which holds that highly chlorinated municipal water and other sanitary protection behaviors reduce a child's early exposure to environmental microorganisms, which could contribute to a slower immune maturation through lack of training. The threshold of tolerance to beta cell antigens decreases, and exposure to various triggers later on can more easily initiate the autoimmune process. If you use a private source (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, but its specific contribution to T1D risk remains modest in 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 bisphenols (BPA, BPS, BPF), phthalates (used in soft PVC, food packaging, scented cosmetics, vinyl toys), persistent organic pollutants, dioxins, certain pesticides, and 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, and cosmetic products not labeled "phthalate-free". These substances migrate more easily into food and beverages in the presence of heat, fat, and acidity. BPA can alter insulin secretion and induce oxidative stress in 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 [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 compared with 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. Refuse thermal paper receipts when you don't need them and wash your hands after touching them. These choices reduce overall chemical exposure, without being specific prevention measures for T1D, 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 fragmentation of larger plastics and through direct shedding from packaging, bottles, synthetic textiles, tires, and cosmetic products. Daily sources of exposure include water bottled in plastic bottles (especially heated or reused), food films, "take-away" containers, baby bottles sterilized at high temperatures, tea bags with plastic fibers, plastic cutting boards, indoor dust, and 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 T1D are still theoretical and come from animal models. They could include disruption of the intestinal barrier ("leaky gut") and dysbiosis, 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), and oxidative stress in the immune system and pancreatic beta cells. 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 bottles. Avoid storing acidic foods, such as tomato sauces or citrus, in plastic containers. Note that the "BPA-free" label does not guarantee safety, since substitutes such as BPS and BPF have similar effects [6].