Asbestos Health Effects : Physiologic Effects, Part 2

by CDC

(Page 5 of 9)

Mesothelioma

Mesothelioma is a signal tumor for asbestos exposure and can appear after relatively low-level exposures.

Mesotheliomas are tumors arising from the thin serosal membranes that surround internal organs. The majority of mesotheliomas are due to asbestos exposure, although the National Cancer Institute (NCI) states that up to 30% have unknown causes. Pleural and peritoneal mesotheliomas are uncommon in the general, unexposed population. Although all asbestos types can cause mesothelioma, several studies have suggested that in humans the amphibole mineral form might be more likely to induce mesothelioma than the serpentine form. Evidence shows that peritoneal mesotheliomas are associated with higher levels of asbestos exposure than pleural mesotheliomas. Unlike asbestos-related bronchogenic cancer, mesothelioma risk does not appear to be influenced by smoking.

Mesothelioma can occur with low asbestos exposure; however, very low background environmental exposures carry only an extremely low risk. The dose necessary for effect appears to be lower for asbestos-induced mesothelioma than for pulmonary asbestosis or lung cancer. However, an extremely short exposure period might be sufficient to cause this rare tumor. A long latency period is typical-a minimum of 10 years from the first exposure is required to attribute the mesothelioma to asbestos exposure. Latency periods have been up to 57 years, although more intense exposures can result in latencies as short as 20 to 30 years. In most cases the latency interval is 30 to 40 years (International Expert Meeting on Asbestos, Asbestosis, and Cancer 1997). Some studies indicate that risk of mesothelioma from a given level of asbestos exposure depends primarily on elapsed time since exposure, with risk increasing dramatically after a lag period of about 10 years.

An estimated 1,500 cases of mesothelioma per year occur in the United States (compared with an average of 130,000 cases of lung cancer per year, mostly due to smoking). Data on death rates from pleural or peritoneal mesotheliomas over the past 10 to 20 years indicate that mesotheliomas are increasing in males over 65 years of age who have histories of occupational exposure to asbestos. Rom (1998) states that the incidence of mesothelioma in the United States is increasing; the incidence of mesothelioma is peaking in their exposure-related mesothelioma incidence from 1940 to 1970. In the United Kingdom, where imports of asbestos peaked in the 1960s and 1970s, a peak in mesothelioma deaths is expected in 2020.

Lung Cancer

Latency for lung cancer is 10 to 30 years or more.

There is little doubt that all types of asbestos can cause lung cancer. A latency period of 10 to 30 years or more exists between the onset of asbestos exposure and occurrence of the tumor. Whether asbestos exposure will lead to lung cancer depends not only on cumulative exposure, but also on other underlying lung cancer risks. The incidence of lung cancer from all causes is high in the general population, so asbestos as a causative factor is difficult to prove in an individual patient. The presence of asbestosis is an indicator of high exposure, but lung cancer can occur in its absence as well. Pleural plaques occur at lower levels of asbestos exposure, and diffuse pleural thickening occurs at moderate to high levels of exposure.

It is unclear whether a threshold asbestos dose exists for lung cancer.

All four major histologic types of lung cancer (squamous cell carcinoma, adenocarcinoma, large-cell carcinoma, and small-cell carcinoma) are associated with asbestos exposure. Although asbestos-associated lung cancer tends to occur in the lower lung fields, histologic type and anatomic location are of no help in determining whether the tumor is due to asbestos. As stated previously, even 1 year of heavy exposure or 5 to 10 years of moderate exposure can increase lung cancer risk twofold or more. The relative risk of lung cancer is estimated to increase 0.5% to 4% for each fiber per cubic centimeter per year (fiber-years) of cumulative exposure (International Expert Meeting on Asbestos, Asbestosis, and Cancer 1997). At very low levels of asbestos exposure, the risk of lung cancer appears to be undetectably low (International Expert Meeting on Asbestos, Asbestosis, and Cancer 1997).

Other Carcinogenic Effects

Increased incidence of GI cancers has been reported among asbestos workers.

Some mortality studies of asbestos workers have revealed small increases in the incidence of death from cancer at one or more extrathoracic sites, including the larynx, the kidneys and the GI system-notably the esophagus, stomach, colon, and rectum. Presumably, these cancers (other than the larynx) are due to swallowing asbestos fibers.

The consequences of ingesting asbestos fibers are a subject of controversy.

In contrast, other epidemiologic studies have not detected statistically significant associations between asbestos ingestion and extrathoracic cancers. Various researchers and regulatory groups have reviewed the weight of evidence and have not been able to reach a consensus on the effects of ingested asbestos fibers. Whether GI neoplasms can be induced by ingesting asbestos-contaminated drinking water (or other ingestion sources) remains controversial. In humans, asbestos bodies have been identified in extrapulmonary tissues including tonsils, thoracic and abdominal lymph nodes, pleura, peritoneum, liver, spleen, kidneys, adrenals, small intestine, pancreas, and bone marrow, as well as the lungs. In any case, oral exposure to asbestos should be avoided.

Cardiovascular Effects

Cardiovascular effects are secondary to pulmonary fibrosis.

Fibrosis of the lung can lead to increased resistance to blood flow through the capillary bed, resulting in cor pulmonale. This condition can also occur with less severe fibrotic disease, especially if chronic obstructive lung disease is simultaneously present, as commonly seen in cigarette-smoking asbestos workers. Pulmonary hypertension can occur before decreased respiratory function is clinically detectable. Limited data from case reports suggest that constrictive pericarditis due to fibrous thickening can also result from asbestos exposure (Agency for Toxic Substances and Disease Registry 2001).

Immunologic Effects

Immunologic abnormalities have been noted in persons with asbestosis.

Immunologic abnormalities have been observed in asbestos workers with clinical signs of asbestosis and have also been reported in environmentally exposed persons. Despite some variability, most studies indicate that cell-mediated immunity can be depressed in workers who have radiologic evidence of asbestosis. Autoantibodies (rheumatoid factor, antinuclear antibodies) are typically present in these workers. Caplan syndrome (the coexistence of pneumoconiosis with rheumatoid changes) also has been noted in asbestos workers, although it is more common in coal miners and workers with other pneumoconiosis. The implications of these immunologic changes are difficult to assess, but they are of special concern because depressed immune function might be a factor in the etiology of asbestos-induced cancer.

About the Author

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