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India, Oct. 30 -- Up to one-third of deaths from heart attack, stroke, lung cancer and chronic respiratory diseases are caused by air pollution, says World Health Organization 'No one [...]

Background: Lung cancer rates in rural Xuanwei County, Yunnan Province, are among the highest in China. Residents traditionally burned 'smoky' coal in unvented indoor firepits that generated very high levels of air pollution. Since the 1970s, most residents have changed from firepits to stoves with chimneys. This study assessed whether lung cancer incidence decreased after this stove improvement. Methods: A cohort of 21232 farmers, born from 1917 through 1951, was followed retrospectively from 1976 through 1992. All subjects were users of smoky coal who had been born into homes with unvented firepits. During their lifetime, 17 184 subjects (80.9%) changed permanently to stoves with chimneys. A hospital record search detected 1384 cases of lung cancer (6.5%) during follow-up. Associations of stove improvement with lung cancer incidence were analyzed with product-limit plots and multivariable Cox models. In 1995, indoor concentrations of airborne particles and benzo[a]pyrene were compared in Xuanwei homes during smoky coal burning in stoves with chimneys and in unvented stoves or firepits. Results: A long-term reduction in lung cancer incidence was noted after stove improvement. In Cox models, risk ratios (RRs) for lung cancer after stove improvement were 0.59 (95% confidence interval [CI] = 0.49 to 0.71) in men and 0.54 (95% CI = 0.44 to 0.65) in women (for both, P

In this study, the authors investigated regional differences in lung cancer mortality in Japan, and, based on data acquired between 1970 and 1990 for 47 Japanese prefectures, estimated the relationship between regional lung cancer mortality and air pollution and/or temperature. Investigators used data for nitrogen dioxide, sulfur dioxide, motor vehicle density, tobacco expenditure, and temperature as independent variables for age-adjusted lung cancer death rates. The age-adjusted lung cancer death rates were higher in the southern geographical block of Japan (i.e., approximately 1.2-fold in males and 1.1-fold in females) and in the northern block (approximately 1.2-fold in males) than in the central block. The regional differences in the age-adjusted lung cancer death rates were explained by nitrogen dioxide and temperature. Temperature caused a greater effect (regression coefficients) of nitrogen dioxide on the age-adjusted lung cancer death rates than did nitrogen dioxide alone in the southern block (i.e., approximately 1.3-fold in males and 1.2-fold in females). These results provide the first evidence of a possible synergistic interaction between air pollution and high temperature on lung cancer mortality., Lung cancer mortality has increased continuously in Japan. Standardized death rates in Japan were 45.3 in males and 11.9 in females per 100 000 population in 1991; these rates were [...]

Satisfactory surveillance of the work environment and employee health presents a major challenge. The usual approaches to minimize worker exposure to suspected carcinogens in the ambient environment are no longer satisfactory. These approaches fail to consider the influence of intermediary processes between exposure and the development of the cancer. Furthermore, for employees exposed to many potential carcinogens, biological markers and biologically effective exposures and doses must be determined for each compound. Chemical carcinogens exert their effects by producing either direct genetic damage or secondary damage that alters potential genetic expression. Compounds in the work environment may affect oncogenes (genes that stimulate the transformation of the host cell to a cancer cell) or antioncogenes (tumor suppressor genes). It is known that no single gene alone is responsible for the transition from normal to malignant cell type. The transition process after exposure to chemical carcinogens to the development of tumor depends on the action and interaction of certain oncogenes and antioncogenes. One such oncogene is the ras oncogene, which is know to be activated in the development of many human cancers, especially lung cancer. Malignancies are also associated with exposure to chemical carcinogens, such as the polycyclic aromatic hydrocarbons (PAHs). The PAHs are products of high temperature combustion of carbon-containing compounds, and are in cigarette smoke and are products of the coal and coke, iron and steel, rubber tire, and petroleum industries. The ras oncogene can be activated by specific point mutations produced by the action of these compounds. As with other genes, the ras oncogene exerts a specific influence through the expression of a specific protein product, p21. There is evidence of ras oncogene activation and p21 expression in human lung cancers. The detection of the ras oncogene/p21 in these cases suggests that they may be useful as a cancer biomarker for individuals exposed to respiratory carcinogens. (Consumer Summary produced by Reliance Medical Information, Inc.)

Radon is a radioactive gas produced by the decay of uranium, a natural element found in rocks and soil. High levels of radon exposure, such as the levels encountered by uranium miners, are associated with lung cancer. The association between uranium mining and lung disease was made over 100 years ago in Europe. In the 1950's, an increased number of lung cancer cases was noted in Colorado uranium miners, and a program was started to measure exposure and monitor the miners' health. The program continues to track these data, and has found excess cancer deaths of 0.3 to almost 13 percent. Since uranium occurs naturally in soil, it has long been suspected that radon might be a risk factor for lung cancer among the general population. While radon released outdoors is diluted by the atmosphere, radon released indoors, which comes from the soil surrounding the foundation of a house, is undiluted and accumulates in the air. Most surveys of radon exposure in homes began around 1980, and higher radon levels were associated with geographic areas. There are several different types of radon test kits for home use, but many are not entirely accurate. The EPA recommends that levels of radon above 4 picocuries per liter (pCi/L) be avoided, and estimates that 5,000 to 20,000 excess cases of lung cancer may result from exposure to radon above these levels. It is also estimated that 2 to 10 million homes in the US may contain radon levels above 4 pCi/L. However, there are few simple methods to effectively reduce radon levels, and reducing radon in the home is up to the homeowner. General methods include preventing radon from entering the home, diverting it once it has entered, or removing the radon. Sealing off the home is not always effective, and diverting the radon through subfloor ventilation, although effective, can be expensive. Using a fan to vent the radon to the outside may actually draw more radon into the house. Now that public awareness has been focused on radon, testing is now required in some areas when buying or selling a house. In addition, better construction practices in new homes may reduce the level of indoor radon exposure. (Consumer Summary produced by Reliance Medical Information, Inc.)

WHO cancer agency concludes exposure to air pollution causes lung cancer The specialized cancer agency of the World Health Organization (WHO), the International Agency for Research on Cancer (IARC), announced [...]

Lung cancer is the principle cause of morbidity and mortality from cancer in the developed countries, and several epidemiological studies show its relation to environmental exposure in urban industrial areas. [...]

For the past ten years formaldehyde has been considered a possible carcinogen, a cancer-causing agent. In 1986 Blair et al published in the Journal of the National Cancer Institute a study of a large number of industrial workers exposed to formaldehyde, and concluded that excesses in deaths from lung cancer were not related to formaldehyde exposure. In 1988, in the Journal of Occupational Medicine, Sterling et al reanalyzed the same data and concluded that exposure to formaldehyde had a cumulative effect and was indeed related to high rates of lung cancer, as well as other cancers and other causes of death. In the November, 1989 Journal of Occupational Medicine, Blair et al questioned the reanalysis by Sterling. In this article the authors respond to Blair et al, claiming that Blair had not, as he had stated in his rebuttal, masked the death rates from cancer, but that he had denied a relationship with formaldehyde exposure and lung cancer. The analysis done by Sterling et al questioned the validity of the exposure measurement done in the factories as reported by Blair. The authors correct a calculation error in their original reanalysis. Their final conclusion is that there is an elevated risk for lung cancer due to cumulative exposure to formaldehyde. Because of rectification of the calculation error, they no longer find an elevated risk to all causes of death or all cancers from formaldehyde.

The environment in steel foundries was studied to determine the causes of lung cancer. Mutagenic levels were higher in the foundries than in urban air. It is felt that avoiding smoking, reducing particulate and usage of particulate respirators are all measures that should be considered until the risk is fully understood.