Heat, Humidity and Pollution: New Study Probes the Environmental Triggers of Hidradenitis Suppurativa

Hidradenitis suppurativa has long been one of dermatology’s most punishing and least understood diseases. It produces painful, recurrent nodules and abscesses in the armpits, groin and other areas rich in apocrine glands and hair follicles, and for many patients it flares for years before anyone attaches a name to it. The condition affects an estimated one percent or more of the population, carries a heavy burden of pain, drainage, scarring and social isolation, and is strongly associated with smoking, obesity and metabolic disease. Yet for all that clinicians know about who develops the disease, surprisingly little is known about where and under what environmental conditions it flourishes. A new research letter published in the Archives of Dermatological Research by a team at the University of Nebraska Medical Center sets out to close part of that gap by asking a deceptively simple question: what, if anything, does the outside world have to do with it?

The study, led by Gunther Grinde and Megan Lorenz as co-first authors with senior authorship shared by Kaeli Samson and Erin X. Wei, was conducted as a single-center analysis at the University of Nebraska Medical Center in Omaha. The researchers reviewed records of patients with hidradenitis suppurativa seen at their institution and linked the clinical picture to environmental exposure data drawn from existing, publicly available sources. That pairing of a real-world patient population with objective environmental measurements is what gives the work its interest. Most of what dermatologists know about triggers of the disease comes from patient self-report, small surveys or mechanistic speculation, rather than from systematic comparisons of disease patterns against measured conditions such as temperature, humidity or air quality.

The rationale for looking outward, rather than only inward at the skin itself, rests on a growing body of literature connecting environmental stressors to inflammatory skin disease. A 2025 meta-analysis in JAMA Dermatology synthesized evidence that climate conditions, weather changes and air pollutants are associated with flares of atopic dermatitis, another chronic inflammatory disorder of the skin. Separate reviews have catalogued the mechanisms by which particulate air pollution and climate change damage the skin barrier, alter the microbiome and drive oxidative stress and inflammatory signaling. If pollution and weather can measurably worsen one chronic inflammatory skin disease, the Nebraska team reasoned, it is plausible that they influence hidradenitis suppurativa as well, a disease whose flares many patients anecdotally link to heat, sweating and friction.

The biology behind that suspicion is worth unpacking. Hidradenitis suppurativa is now understood as a disease of the hair follicle, in which follicular occlusion, immune dysregulation and dysbiosis of the skin microbiome combine to produce deep, painful inflammation. Sweat and moisture are central to this cascade. Occluded, damp skin favors bacterial overgrowth and maceration, and apocrine gland-rich regions are precisely where sweat accumulates. Heat and humidity increase sweating; friction from clothing and skin-on-skin contact compounds follicular trauma. Airborne pollutants, meanwhile, can adhere to sweat and sebum on the skin surface, generating reactive oxygen species and disrupting the barrier. In theory, then, a hot, humid, polluted environment should be close to a worst-case scenario for someone predisposed to the disease, and cooler, drier conditions should be more forgiving.

Nebraska offers an interesting natural laboratory for testing such ideas. The state sits in the continental interior, with hot summers, cold winters, wide seasonal swings in humidity and a largely rural and agricultural landscape punctuated by urban centers. Patients seen at a single academic center there will have experienced a broad range of weather and, potentially, differing exposures to agricultural dust, pollen and urban pollution. By anchoring the analysis to one institution, the researchers could reduce some of the confounding that plagues multi-site studies, where differences in diagnostic practice, coding and patient demographics between centers can swamp the environmental signal they are trying to detect. The tradeoff, which the authors acknowledge implicitly by framing the work as a research letter rather than a definitive study, is that a single center’s patient mix may not generalize to other regions or populations.

The methodological architecture of the study reflects this tension between rigor and feasibility. The protocol was reviewed and approved by the University of Nebraska Medical Center Institutional Review Board, with patient consent waived, and the study was conducted in accordance with the Declaration of Helsinki. Patient-level data were not made publicly available because of institutional restrictions and privacy considerations, while the environmental data were obtained from publicly available sources. The statistical analysis was performed by the biostatistics team, and the work was supported in part by the institutional READi biomedical informatics core, which is funded through the National Institutes of Health, the Patient-Centered Outcomes Research Institute and the Nebraska Research Initiative. In other words, this is a carefully governed, modestly resourced study designed to generate hypotheses rather than to settle them.

Why does this kind of hypothesis-generating work matter for patients? Hidradenitis suppurativa is notoriously difficult to manage. Available treatments, from antibiotics and hormonal therapies to biologic drugs that block tumor necrosis factor, help many patients but rarely produce complete, durable remission, and surgical options are reserved for advanced disease. If modifiable environmental factors, such as exposure to extreme heat, high humidity or poor air quality, measurably influence disease activity, they would represent levers that patients and clinicians could actually pull. Counseling a patient to manage sweating, choose breathable clothing or use air filtration during pollution episodes is far cheaper and safer than escalating immunosuppressive therapy, and it aligns with the broader movement in dermatology toward lifestyle and environmental counseling as adjuncts to pharmacologic treatment.

The study also arrives at a moment when the intersection of climate and skin health is moving rapidly up the research agenda. Recent reviews have argued that rising temperatures, shifting humidity patterns, increased ultraviolet exposure and worsening air quality constitute a slow-moving public health problem for the skin, with chronic inflammatory conditions likely to bear a disproportionate share of the burden. For hidradenitis suppurativa specifically, a disease already linked to daily lifestyle factors such as smoking, diet, obesity and sweating, climate change could plausibly shift the geography of flares, lengthening the hot, humid seasons during which patients suffer most. Studies that establish baseline associations between the disease and measured environmental variables are the necessary first step toward projecting those future impacts and designing adaptation strategies for vulnerable populations.

It is equally important to read the findings with appropriate caution. Single-center analyses are vulnerable to selection bias: the patients who reach an academic dermatology clinic in Omaha are not a random sample of everyone with the disease, and referral patterns, insurance status and distance to care all shape who appears in the dataset. Environmental exposure assigned by residence or by the location of the treating center is a crude proxy for what any individual patient actually experiences, since people spend most of their time indoors, travel between climates and differ in occupation, activity level and air-conditioning access. Confounding by socioeconomic factors, which are themselves strongly tied to both disease severity and environmental exposure, is a persistent threat in this literature. The authors declare no conflicts of interest and are transparent about the scope of their data, but the honest conclusion is that environmental associations of hidradenitis suppurativa remain, at this stage, a promising frontier rather than an established clinical fact.

What the Nebraska study ultimately contributes is momentum and a template. By demonstrating that it is feasible to link a well-characterized single-center cohort of hidradenitis suppurativa patients to publicly available environmental data, and by doing so under formal ethical oversight with professional biostatistical support, the team has laid groundwork that larger, multi-center and longitudinal studies can build upon. The logical next steps are clear: follow patients prospectively across seasons, measure exposures at the individual level, and test whether environmental variables predict flares independently of the established risk factors of smoking and obesity. If those studies confirm what this analysis hints at, the management of one of dermatology’s most burdensome diseases may gain a new dimension, one that treats the patient’s environment, not just their skin, as a legitimate target of care.

Subject of Research: Environmental factors associated with hidradenitis suppurativa

Article Title: Environmental associations of hidradenitis suppurativa: a single center analysis

Article References: Grinde, G., Lorenz, M., Kumar, E. A., McGrath, J., Sharma, D., Zhan, Y., Samson, K., & Wei, E. X. (2026). Environmental associations of hidradenitis suppurativa: a single center analysis. Archives of Dermatological Research, 318(1), Article 424. https://doi.org/10.1007/s00403-026-04882-3

Image Credits: AI Generated

DOI: 10.1007/s00403-026-04882-3

Keywords: hidradenitis suppurativa, dermatology, environmental health, air pollution, climate, heat stress, humidity, skin barrier, chronic inflammation, single-center study, University of Nebraska Medical Center, Archives of Dermatological Research