To inform estimates of risk across the full range of concentrations, we used the approach of Pope and colleagues132 and integrated epidemiological evidence for the hazardous effects of particulate matter at different concentrations from different sources and environments. Methods for estimation of the integrated exposure– response curves for each cause are described elsewhere.138 Briefly, we compiled study-level estimates of the RR of mortality associated with any or all of ambient air pollution, second-hand smoke, household air pollution, and active smoking for the following outcomes: ischaemic heart disease, stroke, lung cancer, chronic obstructive pulmonary disease, and acute lower respiratory tract infection in children. We evaluated several non-linear functions with up to three parameters for fitting the integrated exposure– response relation and assessed them by calculation of the root mean squared error. An exponential decay with a power of concentration was the functional form that provided the best fit for all five outcomes. The integrated exposure–response curve was then used to generate effect sizes specific to the amount of ambient particulate matter smaller than 2·5 µm for each population. For ischaemic heart
