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Environmental Pathology
These environmental disorders are significant because most are
preventable through public health and personal measures.
Etiological agents
The list of causative agents is very long, however, it includes
1. Nutritional factors
2. Air pollutants including tobacco smoking
3. Chemicals including drugs
4. Physical factors including ionizing radiation.
Air pollution refers to loading the atmospheric air with noxious
gases, fumes, and particles etc.
Pollutant: is an agent in the environment that can cause disease in
those who are exposed.
AIR POLLUTION
Air pollution is worst in industrialized areas; the lungs are affected more
than any other system.
Air pollution in general and cigarette smoking in particular contribute to
the causation and aggravation of many lung diseases.
Examples of environmental lung diseases:
1. COPD (COAD) (chronic obstructive pulmonary or airway diseases
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):
chronic bronchitis and emphysema
2. Laryngeal inflammation
3. Pneumoconiosis caused by specific dusts.
The pulmonary changes in cases of air pollution range from
1. Minor irritations
2. Debilitating fibrotic diseases
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COAD refers to conditions in which there are chronic limitations to air flow in the lungs. Flow
is reduced for one of two reasons
1. Airways resistance is increased by narrowing of the air passages or
2. Outflow pressure is reduced (elastic recoil of lungs are lost e.g. in emphysema.
The main diseases in this category are chronic bronchitis asthma and emphysema
The main risk factor for this group is lifetime smoking exposure. (and asthma in childhood)
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3. Cancer.
Factors that determine the injurious potential of air
pollutants
1. Water solubility. Water-soluble molecule (for e.g. SO
2
) dissolved
in the secretions of the upper air passage.
2. Particle size.
Particles that are 0.5 micron in diameter act like gases and move in
and out of alveoli.
Those that are 1-5 micron in diameter are the most dangerous
because of their impaction at the distal airway passages. There they
are engulfed by macrophages and neutrophils that then release
mediators (e.g. macrophage inflammatory protein) that lead to
inflammatory reaction.
Particles greater than 5-10 microns in diameter are unlikely to
reach distal airways; they are filtered out in the nose or trapped and
evacuated by the muco-ciliary movement of the lining epithelium.
3. Concentration. This is directly related to the effects that the agent
produces.
SO2 depending on its concentration may produce the following
Effects :
Less than 0.2 ppm
eye irritation.
2-5 ppm (part per million)
increases airway resistance.
More than 20 ppm
decrease in muco-ciliary clearness
and may cause pulmonary edema
4. Duration of exposure. The longer the period of continuous
exposure to a pollutant present in air, the greater its accumulation
in the lung and hence its noxious effects.
5. Reactivity of the pollutant. Coal dust is relatively inert, and
large amounts must be deposited in the lungs before lung
disease is clinically apparent. Silica, asbestos and beryllium
are more reactive than coal dust, resulting in fibrosis within
the lung tissue at lower concentrations.
6. Host clearance mechanism. Impaired capacity to clear
inhaled particles that occur in some lung diseases (such as
emphysema, chronic bronchitis) leads to higher accumulation
of potentially toxic substances in lung.
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TOBACCO SMOKE
Of all air pollutants, tobacco smoke is the one associated with the highest
prevalence of diseases. 50% of all cigarette smokers will die of smoking
related diseases.
Substances present in cigarette smoke include carcinogens and tumor
promoters.
Carcinogens include
1. Tar
2. Polycyclic aromatic hydrocarbons
3. Benzopyrene
4. Nitrosamine
Promoters include
1. Nicotine
2. Phenol
Cigarette smoking is by far the commonest cause of chronic
obstructive airway diseases (chronic bronchitis and emphysema) as
well as, the most serious of all, lung carcinoma. All these are common
diseases nowadays.
Agents in smoke have a direct irritant effect on the tracheo-bronchial
mucosa, producing inflammation & increase mucus production.
Cigarette smoke results in recruitment of leukocytes to the lung with
increase in local elastase production from these inflammatory cells and
subsequent injury and damage to lung elastic tissue. The ultimate effect is
the development of emphysema as a result of loss of the elastic recoil of
lung tissue.
Atherosclerosis and its complications such as myocardial infarction are
strongly linked to cigarette smoking. This is due to
1. Acceleration of the process of atherosclerosis that leads to
narrowing of the arterial lumen and hence myocardial ischemia.
2. Increased platelets aggregation with subsequent thrombotic
occlusion of the arterial lumen that is already narrowed by
atherosclerosis.
3. Decreased myocardial oxygen supply due to
- Significant lung disease interfering with proper oxygenation
of blood
- Carbon monoxide content of the smoke leading to hypoxia
4. Increased oxygen demands.
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Smokers are more liable for ventricular fibrillation that is why the
incidence of sudden death is much higher in smokers compared to
nonsmokers.