ESTIMATING THE EFFECT OF DIETARY-FAT ON THE RISK OF LUNG-CANCER IN NONSMOKING WOMEN

In 1992, approximately 13 000 lung cancers occurred in nonsmoking U.S. women but the cause of these highly fatal tumors is not well understo od. As the rate of smoking declines in many developed countries, the i nterest in identifying lung cancer risk factors other than tobacco smo king is increasing. A population-based, case-control study of incident lung cancer among nonsmoking women in Missouri was conducted between 1986 and 1992 to assess the effect of a comprehensive list of potentia l risk factors. Dietary information on 429 case subjects and 1021 cont rol subjects was obtained by personal interview, or next-of-kin interv iews (36% and 64%, respectively) and the relationship of diet to lung cancer risk is the focus of this investigation. Odds ratios and popula tion attributable risks (PAR) for dietary fat and dietary saturated fa t were computed among lifetime nonsmokers and long-term ex-smokers. Th e mean age at lung cancer diagnosis was 71 years old, and nearly 50% o f the lung cancers were histologically confirmed adenocarcinomas. Diet ary intake of saturated fat was the leading identified cause of lung c ancer among lifetime nonsmokers and former smokers in Missouri. The et iologic link between dietary saturated fat and lung cancer has not bee n examined in many other studies and the studies published to date are not completely consistent with the hypothesis so a cautious interpret ation of the population attributable risks for these exposures is warr anted. Nonetheless, a growing number of studies arising from around th e world purport to show a link between fat, saturated fat and/or chole sterol or food groups containing relatively high amounts of these macr onutrients (i.e. dairy products, eggs and/or red meat consumption) and lung cancer, and these recent studies add support to this hypothesis. If the results from Missouri are valid and applicable to other Americ ans, 23% of lung cancer cases among lifetime nonsmokers in the United States could be prevented if the saturated fat consumption of the uppe r half of saturated fat intake continuum could be reduced to the level consumed by the lower half. Even greater reductions in risk could be achieved if saturated fat consumption were reduced to even lower level s (i.e. 20th percentile of consumption as shown in this paper). Howeve r, additional etiologic research and evaluation is needed before speci fic dietary recommendations concerning fat and saturated fat and lung cancer prevention can be made.