Toxicological and epidemiological studies of cardiovascular effects of ambient air fine particulate matter (PM_2.5) and its chemical components: Coherence and public health implications

Abstract

Recent investigations on PM_2.5 constituents’ effects in community residents have substantially enhanced our knowledge on the impacts of specific components, especially the HEI-sponsored National Particle Toxicity Component (NPACT) studies at NYU and UW-LRRI that addressed the impact of long-term PM_2.5 exposure on cardiovascular disease (CVD) effects. NYU’s mouse inhalation studies at five sites showed substantial variations in aortic plaque progression by geographic region that was coherent with the regional variation in annual IHD mortality in the ACS-II cohort, with both the human and mouse responses being primarily attributable to the coal combustion source category. The UW regressions of associations of CVD events and mortality in the WHI cohort, and of CIMT and CAC progression in the MESA cohort, indicated that had stronger associations with CVD-related human responses than OC, EC, or Si. The LRRI’s mice had CVD-related biomarker responses to . NYU also identified components most closely associated with daily hospital admissions (OC, EC, Cu from traffic and Ni and V from residual oil). For daily mortality, they were from coal combustion (, Se, and As). While the recent NPACT research on PM_2.5 components that affect CVD has clearly filled some major knowledge gaps, and helped to define remaining uncertainties, much more knowledge is needed on the effects in other organ systems if we are to identify and characterize the most effective and efficient means for reducing the still considerable adverse health impacts of ambient air PM. More comprehensive speciation data are needed for better definition of human responses.

• Annual mortality
• aortic plaque
• cardiac function
• cardiovascular effects
• daily mortality
• hospital admissions
• ischemic heart disease
• particle speciation PM_2.5

Acknowledgements

NYU’s NPACT program involved my extensive collaboration with colleagues at NYU and at other research laboratories. I especially acknowledge the roles of Dr. Kazuhiko Ito (PI for the NPACT time-series epidemiology), Dr. George Thurston (PI for the NPACT annual mortality epidemiology), Dr. Lung-Chi Chen (PI for the NPACT subchronic mouse inhalation exposures), and Dr. Terry Gordon (PI for the NPACT in vitro and in vivo lung aspiration exposures). I would also like to acknowledge the contributions made by the numerous CRT peer reviewers, and by Dr. Sverre Vedal. Their questions for clarifications and suggestions for additional information stimulated me to re-think the content of this paper and to thereby improve it.