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Some recent discussions of adverse human health effects of active and passive smoking have suggested that low levels of exposure are disproportionately dangerous, so that "The effects of even brief (minutes to hours) passive smoking are often nearly as large (averaging 80% to 90%) as chronic active smoking" (Barnoya and Glantz, 2005). Recent epidemiological evidence (Teo et al., 2006) suggests a more linear relation. This paper reexamines the empirical relation between self-reported low levels of active smoking and risk of coronary heart disease (CHD) in public-domain data from the National Health and Nutrition Examination Survey (NHANES). Consistent with biological evidence on J-shaped and U-shaped relations between smoking-associated risk factors and CHD risks, we find that low levels of active smoking do not appear to be associated with increased CHD risk. Several methodological challenges in epidemiology may explain how model-derived estimates can predict low-dose linear or concave dose-response estimates, even if the empirical (i.e., data-based) relation does not show a clear increased risk at the lowest doses. [ABSTRACT FROM AUTHOR]

The hypothesis of hormesis - that substances that harm health at high exposures can reduce risks below background at low exposures, e.g., if they activate defenses without overwhelming them - becomes important for practical policy making if it holds for regulated substances. Recently, the U.S. EPA concluded that reductions in ambient concentrations of fine particulate matter (PM2.5) in air caused trillions of dollars worth of human health benefits for a compliance cost of only about $65 billion per year. This conclusion depends on an unverified assumption of a positive, causal, straight-line relation between PM2.5 concentrations and mortality risks. We review empirical data on PM2.5 and mortality risks (and their precursors, inflammatory responses) and conclude that the PM2.5 concentration-response relation may be J-shaped, rather than linear. This possibility implies that the 1990 Clean Air Act Amendment may well have produced no (or negative) human health benefits, rather than the trillions of dollars worth of reduced mortalities ascribed to it by EPA; and that attempts to achieve further risk-reduction benefits by further reducing PM2.5 concentrations may be counterproductive. This creates a very high value for scientific information that better reveals the true shape of the PM2.5 concentration-response function at and below current ambient levels. [ABSTRACT FROM AUTHOR]