Asbestos Health Effects : Physiologic Effects

by CDC

(Page 4 of 9)

Asbestos primarily affects the respiratory system. The immune and cardiovascular systems, and possibly the GI system, are also affected by asbestos exposure.

The respiratory, immunologic, cardiovascular, and GI systems might be adversely affected by asbestos inhalation and by ingestion of contaminated media or subsequent to mucociliary removal from the respiratory tract. Skin nodules (corns) from handling asbestos-containing materials can also occur.

No deaths due to acute exposure to asbestos have been reported, but even brief (<1 year) high exposures increase risk for future disease. Chronic inhalation exposure can cause death due to asbestosis and cancer. The risk of developing asbestos-associated disease continues even after exposure has ceased. Fibrosis in the lung can lead to increased resistance to blood flow through the pulmonary capillary bed, resulting in pulmonary hypertension and compensatory hypertrophy of the right side of the heart.

Immunologic abnormalities, such as increased concentrations of autoantibodies and depressed lymphocyte responsiveness (Immunologic Effects section), are usually mild or absent in persons who have not developed clinical signs of asbestosis. Cardiovascular effects are secondary to pulmonary changes.

Respiratory Effects

Asbestos exposure can result in asbestosis, mesothelioma, or carcinoma.

Inhalation of asbestos fibers can cause parenchymal (lung) asbestosis, pleural asbestosis (now termed "asbestos-related pleural abnormalities"), pleural mesothelioma, and lung carcinoma. All four syndromes can be present in a patient. Exposure to other carcinogens, dose, intensity and duration of exposure, individual susceptibility, and elapsed time since initial exposure (latency) all can play a role in disease development. Short-term high-level or chronic low-level asbestos exposure have been associated with lung cancer, mesothelioma, and pleural disorders; higher doses are more likely to produce parenchymal asbestosis. Even brief or relatively low exposures from work-related, household, and natural sources can induce pleural plaques or mesothelioma. In some circumstances, exposures in household members can approach occupational levels. One year of heavy exposure (e.g., manufacture of asbestos products, asbestos spraying, insulation work with asbestos materials, or demolition of old buildings) or 5 to 10 years of moderate exposure (e.g., construction or shipbuilding) could increase the lung cancer risk twofold or more. In some circumstances of extremely high asbestos exposure, a twofold increase of lung cancer can be achieved with exposure of <1 year (International Expert Meeting on Asbestos, Asbestosis, and Cancer 1997). Smoking and exposure to other toxicants increase the risk of asbestos-associated lung cancer.

Kamp and Weitzman (1997) report that there is general agreement that histologic or radiologic asbestosis is associated with a significant increase in the risk for lung cancer. However, disagreement exists as to whether asbestosis is simply a marker for high-dose exposure, or whether the interstitial fibrosis of asbestosis is the cancer-producing factor. It is also not necessary to have asbestosis to develop asbestos-related lung cancer.

According to Rosenberg (1997) and Kamp and Weitzman (1997), of workers certified as having asbestosis, about 20% died of pneumoconiosis, 39% died of asbestos-related lung cancer; 9% died from mesothelioma, and 32% died from other causes; 50% of the deaths occurred within 10 years after diagnosis.

Asbestosis

Asbestosis is pulmonary fibrosis of the pleura or parenchymal interstitial tissue.

Inhalation of asbestos fibers can lead to a characteristic pneumoconiosis or diffuse interstitial fibrosis, termed asbestosis. Either heavy exposure for a short time or lower level exposure over a longer period may result in asbestosis; some cases have resulted from intense 1-day exposure. The disease can affect the lung parenchyma or pleural tissue. Clinical manifestations typically appear 20 to 40 years after onset of exposure; however, radiologic changes can occur in <20 years.

Parenchymal asbestosis is characterized as a lung disease involving a restrictive pattern, with obstructive features due to small airway disease, as well as gas exchange abnormalities. It is usually associated with higher exposure levels and radiograph changes, but mild fibrosis can occur at lower exposure levels, and pulmonary function changes can occur even without radiographic changes. Mossman and Churg (1998) feel that the development of asbestosis requires heavy exposure, possibly even involving a minimum threshold of about 25 to 100 fibers/mL/year. Latency is inversely proportional to exposure, and is now about 12.6 to 20.2 years; at lower doses, a longer latency would be expected. Smoking can worsen the result of asbestos exposure, possibly because of the increased particle retention (leading to decreased lung defenses) that takes place in smokers.

Asbestosis patients typically have elevated levels of antinuclear antibody and rheumatoid factors and a progressive decrease in total lymphocyte count with advancing fibrosis. Self-perpetuating host responses might affect the progression of fibrosis, even after exposure ceases. Fibroinflammatory patterns other than conventional asbestosis have also been described for workers with occupational exposure to asbestos. Differentiation of treatable diseases from asbestosis is very important. The differential diagnosis might include the collagen vascular diseases, radiation fibrosis, and rheumatoid arthritis.

Pleural plaques have not been shown to be premalignant.

Pleural effects can occur even in the absence of parenchymal asbestosis. The incidence of pleural abnormalities in persons employed in asbestos-related occupations can be high (20% to 60%). Asbestos-related pleural abnormalities are found as pleural plaques, mainly involving the parietal pleura, sometimes with calcification; and diffuse pleural thickening, which is a collective name for pleural reactions involving mainly the visceral pleura. These abnormalities include benign asbestos-related pleural effusions, blunted costophrenic angle, crow's feet or pleuroparenchymal fibrous strands, and rounded atelectasis (International Expert Meeting on Asbestos, Asbestosis, and Cancer 1997). Pleural plaques are oval areas of acellular collagen deposits, usually located bilaterally on the inferior and posterior surfaces of the pleura; they are usually asymptomatic and without clinically important findings. Pleural plaques are not lung cancer precursors, although persons with pleural plaques have an increased incidence of lung cancer. Migration of inhaled asbestos to the pleura is the most likely cause of plaques. In regions where plaques are not endemic, 80% to 90% of the plaques that are radiologically well defined are attributable to occupational asbestos exposures.

Diffuse pleural fibrosis refers to noncircumscribed fibrous thickening of variable cellularity, usually found in the parietal, but mainly the visceral, layers. In occupational asbestos exposures, such diffuse fibrosis is probably a result of benign asbestos pleuritis with effusion; it might or might not be associated with rounded atelectasis. Diffuse pleural thickening, which is observed radiologically, can be associated with mild or, rarely moderate to severe restrictive pulmonary function deficits such as decreased ventilatory capacity.

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