Environmental exposures contribute to breast cancer development through multiple pathways, with endocrine-disrupting chemicals (EDCs) playing a particularly significant role. Compounds like BPA, phthalates, and organochlorines can mimic estrogen or alter hormone metabolism, creating conditions that promote mammary tissue proliferation. Air pollution particulates, specifically PM2.5, have been associated with increased breast cancer incidence in large cohort studies, possibly through inflammatory mechanisms that damage cellular DNA repair systems. The environmental contribution to breast cancer risk represents a substantial public health opportunity often overshadowed by genetic factors. While BRCA mutations account for only 5-10% of cases, environmental exposures may influence the remaining 90% through epigenetic modifications and cumulative toxic burden. The timing of exposure appears critical, with pubertal and pre-menopausal windows showing heightened sensitivity to carcinogenic influences. Current research suggests that reducing exposure to known EDCs through consumer choices and policy interventions could meaningfully reduce population-level breast cancer rates. This environmental angle complements rather than replaces traditional risk reduction strategies, offering a prevention-focused approach that addresses modifiable factors in our immediate surroundings and lifestyle choices.