Taking a look at occupational and environmental pollutants and potential opportunities for intervention.
Chronic obstructive pulmonary disease (COPD) is a general term used for those diseases in which forced expiratory flow is slowed, usually over a period of at least several months. In addition to individuals with chronic bronchitis and emphysema, the definition includes some persons with asthma who have chronic airflow obstruction (as well as those with less common conditions, such as bronchiectasis and upper-airway obstruction). Air pollution, both indoor and outdoor, has been recognized as an important threat to pulmonary health and a significant contributor to COPD over the past several decades.
It is well established that cigarette smoking is a major environmental risk factor for the development of COPD, yet a number of other and, until recently, less well-established risk factors also exist. These include occupational exposures, ambient air pollution, and exposure to secondhand smoke.
Since 1970, carbon monoxide, hydrocarbons, sulfur dioxide, nitrogen oxides, and ozone have been regulated in the United States by the Environmental Protection Agency. The principal components of visible pollution are hydrocarbons and other coated particles emitted by diesel engines. Considerable attention has also been focused on chlorofluorocarbons (CFCs), which are invisible environmental toxins.
CFCs are not dissolved by rain, and they gradually rise to the ozone layer in the stratosphere, about 15 to 30 km above the surface of the earth. This layer has been called good ozone because it serves a useful purpose and does not come into contact with living creatures. CFCs may linger in the ozone layer for centuries while the suns high-energy radiation breaks them down into chlorine atoms. Chlorine atoms are extremely destructive of the ozone layer; one chlorine atom can destroy more than 100,000 ozone molecules. This destructive ability is magnified by the extreme longevity of CFC molecules.
Scientists now know that a significant ozone hole exists over Antarctica. Ozone levels have also been reduced over North America, Europe, and Australia. Damage to the ozone layer could have dire consequences for life. Ozone functions as a shield to protect surface-dwelling animals and plants against the suns radiationit absorbs most of the harmful ultraviolet radiation before it reaches the earths surface. As ozone depletion accelerates, skin-cancer rates are expected to rise proportionately.
Global warming and increased ultraviolet radiation may lead to an increase in inhaled ozone. The formation of this harmful ozone may result in a higher incidence of airway problems, particularly in airway-sensitive patients such as those with asthma and COPD. Ozone is a potent oxidant that damages the eye and the airway mucosa by activating inflammatory-cell activity through a cytokine-mediated mechanism.
Though largely eliminated from commercial applications such as air conditioning and refrigeration, CFCs are still being used in pressurized metered-dose inhalers (MDIs). It is ironic thatthrough the use of CFC propellantsMDIs may indirectly contribute to the airway damage that their use is intended to prevent.
Overall, the contribution to the CFC atmospheric load from medical inhalers represents less than 1%. Nonetheless, due to increasing concerns over adverse environmental effects of CFCs, guidelines in most countries are restricting and phasing out the use of these chlorine-based propellants. In accordance with the 1989 Montreal Protocol, an agreement signed by 140 nations, a complete phaseout of CFCs for medical inhalers is targeted for 2005. The US Food and Drug Administration has indicated that it intends to comply with the Montreal Protocol.
Since January 1996, all domestically manufactured and imported CFC-containing MDIs intended for commercial purposes have been banned. The only exceptions to the ban are products that are considered medically essential, and these include MDIs used to treat asthma and COPD. Consequently, the CFCs in medical inhaler sprays are believed to be the only significant remaining source of stratospheric ozone depletion.
Occupational asthma is now the most common form of occupational lung disease in industrialized countries. In the United States alone, roughly 2% to 5% of asthma patients (about 600,000 people) have disease attributable to workplace exposure.1 Worldwide prevalence may be even higher, with estimates ranging from 2% to 15%.2
More than 200 agents have been shown to cause occupational asthma and COPD. This number is likely to grow as new chemical agents are introduced into the workplace. Agents that cause occupational asthma include both naturally occurring and synthetic compounds (Table 1). Some authorities divide the agents that can cause occupational asthma into two groups: immunoglobulin E (IgE) dependent and IgE independent. IgE-dependent occupational asthma has a longer latency period between exposure and the onset of symptoms than does IgE-independent occupational asthma. Patients allergy histories, and whether they smoke, are important determinants of susceptibility to occupational asthma developing through IgE-dependent mechanisms. Allergy and smoking histories are less important determinants of occupational asthma developing through IgE-independent mechanisms.3
Although the list of etiologic agents for occupational asthma includes more than 200 items and is growing, only a few of these agents have been extensively studied. These include diisocyanates, epoxy resins, and wood dusts. Epoxy resins are made from acid anhydrides such as phthalic anhydride, tetrachlorophthalic anhydride, maleic anhydride, and trimetallic anhydride. They have a wide range of application in reinforced plastics, adhesives, molding resins, and surface coatings. They are potent irritants, and it is usually difficult to distinguish between allergic and irritant mechanisms. Roughly 40% of epoxy resin workers develop specific IgE antibodies to anhydride protein, and 20% develop respiratory disease associated with the immunologic reaction.4
Wood dusts are a common cause of occupational asthma. One of the best studied is the red cedar. The causative agent in this wood dust appears to be plicatic acid. Roughly 4% of exposed workers develop obstructive pulmonary disease.4
Ambient Air Pollution
In contrast to ozone, nitrogen dioxide is found at higher levels indoors than outdoors, primarily in association with the use of gas stoves and kerosene heaters. Outdoor nitrogen dioxide, however, also contributes a significant fraction to indoor levels. Nitrogen dioxide is less reactive than ozone, and because of its low solubility it penetrates to the lung periphery, where more than 60% of it may be deposited. At peak indoor levels of nitrogen dioxide, studies of healthy volunteers have generally failed to show alterations in lung mechanics or evidence of inflammation with short-term exposure to levels from 0.5 to 2 ppm; however, data from animal exposure studies provide evidence that nitrogen dioxide exposure at similar levels impairs host defenses against bacterial challenge.5 Some studies suggest that patients with asthma and those with mild COPD may be particularly sensitive to the adverse effects of nitrogen dioxide on lung function.5
Carbon monoxide from automobile exhaust and secondhand cigarette smoke has been recognized as an important component of ambient air pollution. Even modest increases in carboxyhemoglobin in patients with ischemic heart disease may cause decreased exercise tolerance. Chronic elevations of carboxyhemoglobin in pregnant women caused by cigarette smoking adversely affect fetal health.
The acute increase in cardiac and pulmonary mortality following the increased smoke and air pollution during the great London fog of 1952 stimulated interest in the potential role of air pollution as a predisposing factor for the development of COPD. Holland and Reid6 compared the pulmonary symptoms and lung function of 293 male post-office employees in central London with those of 477 male post-office workers in a rural setting. Smoking intensity was clearly a critical determinant of respiratory symptoms (persistent cough and phlegm) and pulmonary function, but among subjects with matched smoking histories, forced expiratory volume in 1 second (FEV1) was significantly lower in subjects working in an urban setting. Although air pollutants were not quantified, the relatively high level of air pollution in central London was believed to be the likely cause of decreased pulmonary function among urban workers.
In a larger study7 in Southern California, respiratory symptoms and pulmonary function were compared for residents of a region of high air pollution (Glendora) and a region of low air pollution (Lancaster). Air pollutants were quantified at monitoring stations near the study locations. Higher concentrations of sulfates, sulfur dioxide, oxidants, nitrogen dioxide, and total particulates were found in Glendora than in Lancaster. Among both smokers and nonsmokers, a significantly greater percentage of subjects had markedly reduced FEV1 results in the high-pollution area than in the low-pollution area.
Residents of urban areas with high air-pollution levels appear to have an increased frequency of respiratory symptoms and to have slightly reduced pulmonary function. Although the specific pollutants involved have not been firmly established, a causal relationship between air pollution and reduced pulmonary function seems likely.
Passive Smoke Exposure
Passive exposure to tobacco smoke as a form of environmental pollution has received considerable attention in recent years. Tager et al8 found a significant effect of maternal smoking on the rate of growth of FEV1 in children followed prospectively for 7 years. They estimated a 3% reduction in the projected FEV1 attained by a male nonsmoking child exposed to a smoking mother from ages 11 to 16, compared with the nonsmoking child of a nonsmoking mother. Subsequent studies of the effect of maternal smoking during pregnancy showed that tobacco-smoke exposure in utero contributes to significant reductions in pulmonary function as measured after birth.9
Masi et al10 studied the effects of environmental tobacco-smoke exposure in young, nonsmoking adults aged 15 to 35 years. They estimated cumulative environmental tobacco smoke exposure using a questionnaire that assessed exposure at different age periods. In men, a significant relationship between household environmental smoke exposure and forced expiratory flow, midexpiratory phase, was demonstrated.
The deleterious effects of passive-smoke exposure on adults are less well defined than those seen in infants and children, but some negative effect is likely to be present. The magnitude of the effect of environmental tobacco smoke on pulmonary function in healthy adults remains to be more fully elucidated.
Assessment of Exposures
Assessment of exposures is a critical step in evaluating the contribution of the environment to a patients obstructive pulmonary disease. The goals of exposure assessment are to identify the causative agents, minimize future exposures, and prevent the development of further cases of occupational asthma.11 Essential elements of exposure assessment are listed in Table 2.
Specific inhalation-challenge tests using occupational agents can also be performed in the laboratory or in the workplace. When such tests are performed, there should be adequate ventilation to ensure that RCPs will not be exposed to the agent being used for the test.
Opportunities for Intervention
The RCP has an important role in the management of obstructive lung diseases caused or exacerbated by environmental air pollution. Recognition is the first step toward avoidance. By educating patients about possible triggers associated with their occupations and/or environments, the RCP enhances the opportunity for trigger identification.
Surveillance programs are a keystone for prevention. They may identify individuals who are at an increased risk for developing asthma or COPD in the workplace, and they may detect disease at an early stage when intervention options are likely to be successful. The most sensitive health-surveillance programs currently available include preemployment and periodic examinations, immunologic monitoring, and periodic spirometric surveys.11
Cigarette smoking provides, for the smoker, the most intense exposure to pollution of any kind, and it can contribute significantly to the exposure of other people indoors. Measures to encourage smokers to stop smoking and young people not to start smoking in the first place offer perhaps the greatest opportunity for reducing the prevalence of chronic lung disease.
Particular care is required to avoid the exposure of young children to high levels of pollution, whether of outdoor or indoor origin. Not only are there links between such exposures and the occurrence of respiratory illnesses, but these early experiences also may contribute to the development of COPD later in life.
John D. Zoidis, MD, is a contributing writer for RT.
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10. Masi MA, Hanley JA, Ernst P, et al. Environmental exposure to tobacco smoke and lung function in young adults. Am Rev Respir Dis. 1988;138:296-299.
11. American College of Chest Physicians. ACCP consensus statement. Assessment of asthma in the workplace. Chest. 1995;108:1084-1117.