Exposures
Browse environmental exposures in the GENARCH atlas — definitions, proxies, biological systems affected, sensitive developmental windows, and gene–environment interaction highlights. Population-level summaries only; not for individual risk assessment.
Ambient Air Pollution (PM2.5)
PM2.5 (particulate matter with aerodynamic diameter ≤2.5 micrometers) refers to fine inhalable particles that can penetrate deep into the lungs and enter the bloodstream. Sources include combustion (vehicles, power plants, wildfires), industrial processes, and secondary formation from gaseous precursors (e.g., SO2, NOx). PM2.5 composition varies by region but typically includes sulfates, nitrates, ammonium, organic carbon, elemental carbon, and trace metals. The small size enables alveolar deposition and systemic distribution, contributing to respiratory, cardiovascular, and immune effects.
Alcohol
Ethanol consumption from alcoholic beverages. Includes beer, wine, spirits. Dose-dependent effects on liver, cardiovascular system, cancer risk, and neuropsychiatric outcomes. Moderate vs heavy use has different risk profiles.
Diet Quality
Overall dietary pattern and nutritional quality. Includes intake of fruits, vegetables, whole grains, refined carbohydrates, saturated fat, sugar, and ultra-processed foods. Proxy for nutritional exposures affecting metabolic and cardiovascular health.
Endocrine Disrupting Chemicals (BPA, Phthalates)
Synthetic chemicals that interfere with hormone signaling. Bisphenol A (BPA): found in plastics, food packaging, thermal paper; estrogenic and anti-androgenic. Phthalates: plasticizers in PVC, personal care products; anti-androgenic, affect thyroid. Exposure occurs through ingestion, dermal absorption, and inhalation. These compounds may affect development, reproduction, metabolism, and cancer risk. Genetic variants in hormone receptor pathways may modulate susceptibility.
Endotoxin (Farm/Microbial Exposure)
Lipopolysaccharide from Gram-negative bacteria; exposure common in farm environments. Early-life exposure may protect against atopic asthma (hygiene hypothesis).
Greenspace and Natural Environments
Exposure to vegetated land (parks, forests, street trees, gardens) and natural environments. Measured by NDVI (Normalized Difference Vegetation Index), distance to parks, or percentage of green land use. Greenspace is associated with improved mental health, reduced cardiovascular risk, and potentially lower air pollution and heat exposure. Mechanisms may include stress reduction, physical activity promotion, and microbiome diversity. Urban planning and equity in access are modifiers.
Heavy Metals (Lead, Mercury, Arsenic)
Exposure to toxic heavy metals from environmental and occupational sources. Lead: paint, water pipes, soil, industrial emissions; accumulates in bone. Mercury: fish (methylmercury), dental amalgams, industrial; neurotoxic. Arsenic: contaminated groundwater, rice, industrial; carcinogenic. Heavy metals cause oxidative stress, DNA damage, neurotoxicity, and disruption of enzyme function. Susceptibility varies by genetic variants in detoxification and metal-handling pathways.
Obesogenic Environment
Environmental and contextual factors that promote weight gain and obesity. Includes food environment (access, marketing, portion sizes), built environment (walkability, recreation), sedentary behavior opportunities, and socioeconomic factors affecting diet and activity.
Ozone
Ground-level ozone (O3) is a secondary pollutant formed when nitrogen oxides and volatile organic compounds react in the presence of sunlight. It exacerbates respiratory conditions including asthma.
Physical Activity
Bodily movement produced by skeletal muscles that requires energy expenditure. Includes occupational, transport, household, and leisure-time activity. Measured by duration, intensity (e.g., METs), and frequency. Physical activity improves cardiorespiratory fitness, insulin sensitivity, and mental health; reduces risk of obesity, type 2 diabetes, cardiovascular disease, and some cancers. Sedentary behavior is a related but distinct exposure. Genetic variation in fitness and motivation may modify response to activity interventions.
Psychosocial Stress
Chronic or acute stress from social, psychological, or environmental sources. Includes childhood adversity, discrimination, social isolation, financial strain, trauma, and major life events. Affects mental health, behavior, and physiologic stress responses.
Sleep Deprivation and Circadian Disruption
Insufficient sleep duration or quality, and misalignment of sleep with circadian rhythm (e.g., shift work, social jet lag). Short sleep (<7 h in adults) and poor sleep are associated with obesity, type 2 diabetes, cardiovascular disease, and mental health disorders. Circadian genes (e.g., CLOCK, PER, CRY) interact with sleep and light exposure. Adolescence is a period of natural circadian shift and often insufficient sleep; shift work in adulthood increases metabolic and cardiovascular risk.
Prenatal Tobacco Smoke Exposure
In utero exposure to tobacco smoke from maternal smoking during pregnancy. Associated with impaired lung development and increased childhood asthma risk.
Tobacco Smoke
Tobacco smoke exposure from active smoking or secondhand smoke. Contains thousands of chemicals including nicotine, tar, and carcinogens. Sources include cigarettes, cigars, electronic nicotine delivery systems, and environmental tobacco smoke.
UV Radiation
Ultraviolet radiation from sun exposure. Includes UVA and UVB. Primary cause of skin cancer; also enables vitamin D synthesis. Varies by latitude, season, time of day, and behavior.