Lung cancer exposure

Care must be taken in handling radon, as with other radioactive materials. The main hazard is from inhalation of the element and its solid daughters which are collected on dust in the air. Good ventilation should be provided where radium, thorium, or actinium is stored to prevent build-up of the element. Radon build-up is a health consideration in uranium mines. Recently radon build-up in homes has been a concern. Many deaths from lung cancer are caused by radon exposure. In the U.S. it is recommended that remedial action be taken if the air in homes exceeds 4 pCi/1. 

Antimony is not known to cause cancer, birth defects, or affect reproduction in humans. However, antimony has been shown to cause lung cancer in laboratory animals that inhaled antimony-containing dusts and prolonged exposure to antimony can cause irritation of the eyes, skin, lungs, and stomach, in the form of vomiting and diarrhea. Heart problems can also result from overexposure to antimony (33). 

The replacement of asbestos fibers by other fibrous materials has raised similar health issues in relation to substitute materials. However, since lung cancer has a latency period of approximately 25 years, and since the fiber exposure levels in contemporary industries is far lower than those which prevailed half a century ago, the epidemiological data on most substitutes is insufficient. A possible exception is slag fibers for which several studies on worker populations are available over extended periods (44) some results show a substantial increase in lung cancer occurrence. Consequentiy, the toxicity of asbestos substitute fibers remains a subject of active investigation. 

Effects of indoor air pollutants on humans are essentially the same as those described in Chapter 7. However, there can be some additional pollutant exposures in the indoor environment that are not common in the ambient setting. From the listing in Table 23-1, radon exposures indoors present a radiation hazard for the development of lung cancer. Environmental tobacco smoke has been found to cause lung cancer and other respiratory diseases. Biological agents such as molds and other toxins may be a more likely exposure hazard indoors than outside. 

Chronic Pulmonary Toxicity Chronic damage to the lungs may be due to several subsequent exposures or due to one large dose that markedly exceeds the capacity of pulmonary defense, clearance, and repair mechanisms. Chronic pulmonary toxicity includes emphysema, chronic bronchitis, asthma, lung fibrosis, and lung cancer. The single most important reason for chronic pulmonary toxicity is tobacco smoke, which induces all types of chronic pulmonary toxicity, with the exception of fibrosis. 

Polycyclic aromatic hydrocarbons have been classified as human carcinogens because they induce cancers in experimental animals and because smoking and exposure to mixtures of chemicals containing polycyclic aromatic hydrocarbons in the workplace increase the risk of lung cancer in exposed individuals. In experimental animals, benzo(a)pyrene induces cancer in different organs depending on the route of administration.Furthermore, exposure to polycyclic aromatic hydrocarbons commonly occurs in occupations related to traffic (use of diesel engines in transportation and railways). 

Bronchogenic carcinoma A lung cancer associated with asbestos exposure. 

Several toxic effects of inorganic oxides become evident when oxides are inhaled in a finely powdered form. A high concn of powdered oxides can lead to asphyxiation on short exposure or lung cancer at somewhat lower concns if the exposure occurs over a prolonged period. 

The a-tocopherol, P-carotene (ATBC) Cancer Prevention study was a randomised-controlled trial that tested the effects of daily doses of either 50 mg (50 lU) vitamin E (all-racemic a-tocopherol acetate), or 20 mg of P-carotene, or both with that of a placebo, in a population of more than 29,000 male smokers for 5-8 years. No reduction in lung cancer or major coronary events was observed with any of the treatments. What was more startling was the unexpected increases in risk of death from lung cancer and ischemic heart disease with P-carotene supplementation (ATBC Cancer Prevention Study Group, 1994). Increases in the risk of both lung cancer and cardiovascular disease mortality were also observed in the P-carotene and Retinol Efficacy Trial (CARET), which tested the effects of combined treatment with 30 mg/d P-carotene and retinyl pahnitate (25,000 lU/d) in 18,000 men and women with a history of cigarette smoking or occupational exposure to asbestos (Hennekens et al, 1996). 

The majority of people who smoke never develop lung cancer. Genetic risk factors may predispose certain smokers to lung cancer. After adjustments for age, smoke exposure, occupation, and gender, relatives of a lung cancer patient have approximately a twofold risk of developing lung cancer. The... 

The known health effect associated with exposure to elevated levels of radon above the action or guidance level is an increased risk of developing lung cancer. The guideline levels for radon in existing homes are as follows ... 

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