How exposure to environmental tobacco smoke, outdoor air pollutants, and increased pollen burdens influences the incidence of asthma

Abstract

Asthma is a multifactorial airway disease that arises from a relatively common genetic background interphased with exposures to allergens and airborne irritants. The rapid rise in asthma over the past three decades in Western societies has been attributed to numerous diverse factors, including increased awareness of the disease, altered lifestyle and activity patterns, and ill-defined changes in environmental exposures. It is well accepted that persons with asthma are more sensitive than persons without asthma to air pollutants such as cigarette smoke, traffic emissions, and photochemical smog components. It has also been demonstrated that exposure to a mix of allergens and irritants can at times promote the development phase (induction) of the disease. Experimental evidence suggests that complex organic molecules from diesel exhaust may act as allergic adjuvants through the production of oxidative stress in airway cells. It also seems that climate change is increasing the abundance of aeroallergens such as pollen, which may result in greater incidence or severity of allergic diseases. In this review we illustrate how environmental tobacco smoke, outdoor air pollution, and climate change may act as environmental risk factors for the development of asthma and provide mechanistic explanations for how some of these effects can occur.

Figure 1

Hierarchical oxidative stress model in response to DEP exposure: proteome analysis of oxidative stress proteins shows a hierarchical response. Incremental doses of organic DEP extracts induce a series of incremental cellular responses that include increased antioxidant offense, inflammation, and cytotoxicity. At a lower level of oxidative stress (tier 1), antioxidant enzymes are induced to restore cellular redox homeostasis. At an intermediate level of oxidative stress (tier 2), newly expressed proteins often exhibit proinflammatory activity. At a high level of oxidative stress (tier 3), perturbation of the mitochondrial permeability transition pore and disruption of electron transfer result in cellular apoptosis or necrosis. Abbreviations: FADD, Fas-associating protein with death domain; GM-CSF, granulocyte-macrophage colony-stimulating factor; iNOS, inducible nitric oxide synthase; SOD, superoxide dismutase; TNF, tumor necrosis factor; VDAC-1, voltage-dependent anion channel 1.

Figure 2

Peak date of airborne birch (Betula) pollen concentrations in Denmark, 1978–1999. Viborg: Y_m = 122.1; β = −0.67; r = −0.81; p < 0.001. Copenhagen: Y_m = 123.3; β = −0.74; r = −0.92; p < 0.001. Adapted from Rasmussen (2002).

Figure 3

Number of people living in counties with air quality levels above the National Ambient Air Quality Standards (NAAQS) in 2000. Abbreviations: CO, carbon monoxide; Pb, lead. Data from U.S. EPA (2005).