This review summarizes the published literature on the presence of polycyclic aromatic hydrocarbons (PAH) in indoor air, settled house dust, and food, and highlights geographical and temporal trends in indoor PAH contamination. In both indoor air and dust, ΣPAH concentrations in North America have decreased over the past 30 years with a halving time of 6.7±1.9years in indoor air and 5.0±2.3 years in indoor dust. In contrast, indoor PAH concentrations in Asia have remained steady. Concentrations of ΣPAH in indoor air are significantly (p<0.01) higher in Asia than North America. In studies recording both vapor and particulate phases, the global average concentration in indoor air of ΣPAH excluding naphthalene is between 7 and 14,300 ng/m(3). Over a similar period, the average ΣPAH concentration in house dust ranges between 127 to 115,817ng/g. Indoor/outdoor ratios of atmospheric concentrations of ΣPAH have declined globally with a half-life of 6.3±2.3 years. While indoor/outdoor ratios for benzo[a]pyrene toxicity equivalents (BaPeq) declined in North America with a half-life of 12.2±3.2 years, no significant decline was observed when data from all regions were considered. Comparison of the global database, revealed that I/O ratios for ΣPAH (average=4.3±1.3), exceeded significantly those of BaPeq (average=1.7±0.4) in the same samples. The significant decline in global I/O ratios suggests that indoor sources of PAH have been controlled more effectively than outdoor sources. Moreover, the significantly higher I/O ratios for ΣPAH compared to BaPeq, imply that indoor sources of PAH emit proportionally more of the less carcinogenic PAH than outdoor sources. Dietary exposure to PAH ranges from 137 to 55,000 ng/day. Definitive spatiotemporal trends in dietary exposure were precluded due to relatively small number of relevant studies. However, although reported in only one study, PAH concentrations in Chinese diets exceeded those in diet from other parts of the world, a pattern consistent with the spatial trends observed for concentrations of PAH in indoor air. Evaluation of human exposure to ΣPAH via inhalation, dust and diet ingestion, suggests that while intake via diet and inhalation exceeds that via dust ingestion; all three pathways contribute and merit continued assessment.