Conclusion.
Although exposure to polluted air and dyssynchrony have been independently shown to increase the risk for pulmonary, cardiovascular and metabolic injury it is not clear whether dyssynchrony affects air pollution toxicity. A study that shows that the depletion of Bmal1 increased the sensitivity to inhaled nanoparticles [83] supports the idea that circadian dyssynchrony increases the sensitivity to air pollution exposure, whereas combined exposure to concentrated PM2.5 and dim light at night had no additive neurological affects [84]. However, because the exposure to air and light pollution and changes of our sleep pattern are likely to increase due to increasing urbanization and our modern 24-hour x 7-day live style choices, it is essential to investigate in future studies whether circadian dyssynchrony increases the susceptibility to air pollution toxicity. In addition, chronotoxic effects in shift worker have not been studied yet and it is unclear whether shift work-induced circadian dyssynchrony exacerbates the health effects of pollutant exposure although it is know that shift work, which is often accompanied by exposure to pollutants, has acute and chronic health affects [85]. Results from these studies will be essential in assessing whether air pollution exposure exacerbates pulmonary, cardiovascular and metabolic injury in humans with disrupted circadian rhythm. Additional chronotoxicity studies, will inform about specific times in a day when humans are more sensitive to air pollution toxicity. Such studies could help in identifying specific individuals (e.g., those with disrupted circadian rhythms) who might be more sensitive to air pollution exposure and lead to the development of simple and readily implementable preventive strategies (e.g., realigning circadian rhythms) to mitigate against the major harmful health effects of air pollution. They also could lead to targeted approaches that limit air pollution exposures at certain times during the day.
