The lung is a vulnerable target for volatile substances because of its large alveolar surface area, estimated to be about 100 square meters, leading to exposure to large air volumes. Indeed, humans inhale a volume of about 0.5 liters per breath or 8.640 liters per day. Moreover, it is estimated that the cardiac output is about 7.0L/day. This flow traverses a rich pulmonary capillary bed that provides ease of absorption and transport of inhaled toxic materials throughout the body. Thus volatile agents can directly act in the lung and/or in some remote target organ.
The effects of air pollution on health have been recognized from long time. In the past, the majority of air pollution was derived from domestic and industrial burning of fossil fuels. The introduction of legislation to reduce the use of such fuels has changed the composition of air pollutants. At present, fossil fuel-associated pollutants have been replaced by a steady increase in traffic-associated pollutants such as finer, respirable particulates, oxides of nitrogen (NOx), ozone (O3), and volatile organic compounds.
Usually, all inhaled toxins are associated with environmental exposure. This is largely related to an occupation. The toxins may be responsible for causing chronic inflammation, granulomatous lung diseases, immunosuppression leading to a heightened incidence of respiratory infections, as well as cancer (Table I) .
In terms of incidence, the agents producing immune-inflammatory responses (hypersensitivities) are more common than those responsible for irritant reactions or fibrogenesis.
The immune toxins can be classified on the basis of the hypersensitivity mechanism (Table II). Immediate hypersensitivity is associated with IgE-mediated mast cell activation, resulting in the accumulation of eosinophils and Th2 lymphocytes in the airways. Immune-complex mediated hypersensitivity is related to the immune-complex deposition due to excessive antibody production or deficient clearance. T-cell mediated hypersensitivity is elicited by T cells secreting cytokines that activate macrophages.
Additionally, some substances are able to elicit lung injury involving different cells from those of the immune system such as fibroblasts (silicosis and asbestosis). The last substances to be mentioned are those able to enter the body by the lung but causing their effects in different organs (carbon monoxide).
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