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Concentrations of ambient PM2.5 (particulate matter <2.5 microm in aerodynamic diameter) were associated with increased mortality in two prospective cohort studies. In this paper, I assess whether the weight of the evidence supports a causal association. I assumed the study population in each city to have the same exposure; therefore, these are ecologic studies because exposure is at the group level. Health outcome and confounding data are at the individual level. Ambient PM concentrations are inadequate surrogates for personal exposure because they are at the group level and comprise only a small proportion of personal exposure, they change over time, and they constitute only a small proportion of a life span. The strength of association and exposure-response relationships cannot be determined because the ecologic group-level risks of PM2.5 are overestimated 150- to 300-fold based on an analogy with individual-level exposure to inhaled cigarette smoke. Risk estimates may also be high because of confounding from factors such as physical activity and lung function. The evidence is not coherent because the stronger associations are expected to be with morbidity, but instead are with mortality. For example, PM2.5 was associated with mortality but not with measurable reductions in lung function. Biological plausibility is lacking because lifetime exposure of rats to combustion products at concentrations two to three orders of magnitude higher than air pollution levels cause lung overloading but no consistent reduction in survival. Criteria for quantitative risk assessment are not met so the data are not useful for setting air quality standards. The weight of evidence suggests there is no substantive basis for concluding that a cause-effect relationship exists between long-term ambient PM2.5 and increased mortality.ImagesFigure 1Figure 2Figure 3Figure 4Figure 5

The relationship between crystalline silica and lung cancer has been the subject of many recent publications, conferences, and regulatory considerations. An influential, international body has determined that there was sufficient evidence to conclude that quartz and cristobalite are carcinogenic in humans. The present authors believe that the results of these studies are inconsistent and, when positive, only weakly positive. Other, methodologically strong, negative studies have not been considered, and several studies viewed as providing evidence supporting the carcinogenicity of silica have significant methodological weaknesses. Silica is not directly genotoxic and is a pulmonary carcinogen only in the rat, a species that seems to be inappropriate for assessing particulate carcinogenesis in humans. Data on humans demonstrate a lack of association between lung cancer and exposure to crystalline silica. Exposure-response relationships have generally not been found. Studies in which silicotic patients were not identified from compensation registries and in which enumeration was complete did not support a causal association between silicosis and lung cancer, which further argues against the carcinogenicity of crystalline silica.

The diesel exhaust (DE)-lung cancer hypothesis is evaluated. Diesel power became common after World War II, exposure was to traditional diesel exhaust (TDE) before 1988. In the next, 20 years, emissions were modified to new-technology diesel exhaust (NTDE) containing 1% of pre-1988 levels of diesel particulate matter (DPM). Nearly all pre-1990 studies were cohorts with primarily pre-diesel exposures. This review focuses on the proportion of cases with >20 years since initial DE exposure; strength of association; biological gradients; roles of chance, bias, and confounding; and consistency in 13 diesel studies. Five studies had adequate latency, six had a minority of workers with >20 years' latency, and in two studies most workers had inadequate latency. This pattern suggests too few relevant studies for evaluating the DE-lung cancer hypothesis. The 16 highest exposure categories showed 7 with probable associations (relative risk [RR] > 1.5), 7 with improbable or no associations (RRs < 1.2), and 2 with possible associations (RRs 1.2-1.5). This random pattern with many weak RRs does not support the DE-lung cancer hypothesis. Ten of 34 exposure-response (E-R) analyses showed positive trends and 24 had indeterminate or negative trends. This small number of positive biological gradients does not support causality. Weight of evidence suggests 70% of studies are indeterminate, whereas 30% are positive or negative, indicating a lack of consistency. To support a traditional diesel exhaust-lung cancer hypothesis requires more studies with longer follow-up and quantitative E-R analyses.

The role of surface properties, influenced by particle processing, in particle-particle interactions (powder cohesion) is investigated in this study. Wetting behaviour of mefenamic acid was found to be anisotropic by sessile drop contact angle measurements on macroscopic (>1cm) single crystals, with variations in contact angle of water from 56.3° to 92.0°. This is attributed to variations in surface chemical functionality at specific facets, and confirmed using X-ray photoelectron spectroscopy (XPS). Using a finite dilution inverse gas chromatography (FD-IGC) approach, the surface energy heterogeneity of powders was determined. The surface energy profile of different mefenamic acid crystal habits was directly related to the relative exposure of different crystal facets. Cohesion, determined by a uniaxial compression test, was also found to relate to surface energy of the powders. By employing a surface modification (silanisation) approach, the contribution from crystal shape from surface area and surface energy was decoupled. By "normalising" contribution from surface energy and surface area, needle shaped crystals were found to be ∼2.5× more cohesive compared to elongated plates or hexagonal cuboid shapes crystals.

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