Exposomics is the study of the totality of environmental exposures across a lifetime, and their relationship to health. This page sets out the discipline, the mechanisms linking exposure to five chronic conditions, and the literature each mechanism rests on.
Christopher Wild proposed the term in 2005 to name what genomics could not explain: the cumulative record of every environmental exposure a person meets, from conception onward. Where the genome is fixed at birth and readable once, the exposome changes hour by hour and has to be measured where and when a person actually is.
Rappaport and Smith set out the consequence in Science in 2010: if most chronic disease risk is environmental, the measurement problem \u2014 not the biology \u2014 is the limiting factor.
Each entry states the exposure, the proposed physiological pathway, and the literature. Where the evidence is contested or the effect size is small, it says so.
Falling barometric pressure is the most consistently reported weather trigger in migraine cohorts. The proposed pathway is a pressure differential across the sinus and middle-ear cavities altering trigeminal nerve activity. Effect sizes are modest and individual variation is wide — a substantial minority of migraineurs show no weather sensitivity at all.
Fine particulate matter penetrates to the alveoli, where it drives oxidative stress and airway inflammation. Ozone acts on the epithelium directly. Pollen operates through IgE-mediated sensitisation in atopic individuals, and thunderstorm fracture of pollen grains produces respirable fragments that reach deeper into the airway than whole grains.
Heat raises cardiac output as blood is redirected to the skin for cooling, while dehydration increases blood viscosity. Particulate exposure contributes through systemic inflammation and autonomic imbalance. The two combine: cardiovascular mortality rises measurably during heat events, and more so where particulate levels are high at the same time.
Core body temperature must fall for sleep onset; elevated overnight temperature delays it and fragments slow-wave sleep. Night-time noise produces cortical arousals that do not always reach conscious waking but still degrade sleep architecture. Overnight minimum temperature is the better predictor than daytime maximum.
Grass, tree and weed pollen drive IgE-mediated inflammation of the nasal mucosa. Warming has lengthened pollen seasons and raised peak counts across the northern hemisphere, so historical seasonal expectations increasingly misstate present exposure — an argument for dated records rather than seasonal averages.
Peer-reviewed sources only, indexed and retraction-screened. Review articles are marked as such and are never treated as primary evidence.
This page is educational and non-clinical. It describes published research and does not constitute medical advice. Questions about the science, or a correction to anything stated here \u2014 imiya@vasus.ai.