Although many time-series studies have established associations of daily pollution variations with daily deaths, there are fewer at low concentrations, or focused on locally generated pollution, which is becoming more important as regulations reduce regional transport. Causal modeling approaches are also lacking. Researchers used causal modeling to estimate the impact of local air pollution on mortality at low concentrations.
While many time series studies have established associations of daily pollution variations with daily deaths, there are fewer at low concentrations, or focused on locally generated pollution, which is becoming more important as regulations reduce regional transport. Causal modeling approaches are also lacking. The objective of the study was to use causal modeling to estimate the impact of local air pollution on mortality at low concentrations.
Extreme heat events are associated with spikes in mortality, yet death rates are on average highest during the coldest months of the year. Under the assumption that most winter excess mortality is due to cold temperature, many previous studies have concluded that winter mortality will substantially decline in a warming climate.
Decreasing exposure to airborne particulates was previously associated with reduced age-related decline in lung function. However, whether the benefit from improved air quality depends on genetic background is not known. Recent evidence points to the involvement of the genes p53 and p21 and of the cell cycle control gene cyclin D1 (CCND1) in the response of bronchial cells to air pollution.
A large body of epidemiologic literature has found an association of increased fine particulate air pollution (PM2.5) with acute and chronic mortality. The effect of improvements in particle exposure is less clear.
