Abstract

7583 Background: When epidemiologic research first demonstrated an association between cigarette smoking (CS) and lung cancer (LC) in the 1950s, AD comprised about 5% of LCs and was only weakly related to CS. In the 1960s and 1970s, AD increased sharply, and became strongly related to CS. Methods: We conducted an epidemiological and ecological analysis correlating time trends in LC histology with changes in cigarette design and TI actions over the past 30 yrs. We utilized SEER data on 307,797 LCs diagnosed from 1975 to 2003 to analyze time trends of age-standardized incidence rates of each LC subtype: AD, squamous (SQ), small cell, and large cell. Comparisons were drawn based on sex, race, and age. Because SEER contains no data on CS, other sources were utilized to correlate changing histology to time trends in smoking prevalence, the changing cigarette, and TI actions. Results: Among all pts, AD surpassed SQ by 1980–84 to become the most common histology. AD increased 62% from 1975–79 to 1995–99, but fell 8% in 2000–03. SQ peaked in 1980–84 and dropped 35% by 2000–03. AD surpassed SQ in 1985–89 in men, while AD was already most common in women by 1975–79. AD rose 38% in men from 1975–79 to 1995–99, while it doubled in women during this interval. Among whites, AD surpassed SQ by 1980–84, although this did not occur among blacks for another decade. Nonetheless, AD incidence has consistently been higher in black men than in other subgroups. AD was already most common in pts <50 yrs by 1975–79, while AD rapidly increased and surpassed SQ in all other age groups by 1990–94. By 2000–03, AD comprised 47% of all LCs (42% in men; 52% in women; 59% in pts <50 yrs). Currently, AD is the most common histology in both sexes, races, and in all age groups. Trends in AD correlate with the wide-scale adoption by smokers of filtered and low tar cigarettes, and with increasing nitrosamine levels in cigarettes. Conclusions: The rise of AD, particularly in women and younger persons, is consistent with the hypothesis that changes in cigarette design and composition was responsible for this rise. These changes were introduced by the TI in response to mounting evidence that CS caused other forms of LC. While low tar cigarettes do not reduce LC risk, their adoption appears to be responsible for creating an epidemic of smoking-related lung AD. No significant financial relationships to disclose.

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