Vutuc C
Zentralbl Bakteriol Mikrobiol Hyg B. 1982 Aug;176(4):329-38.
Smoking habits of 297 female lung cancer patients (Kreyberg I: 202, Kreyberg II: 95) and 580 controls were analyzed. In addition tar exposures (TE) were calculated. Calculation of TE includes amount of consumptions, duration and the tar yields of all cigarette brands ever smoked. These are significant more smokers among patients (63%) and patients with a K I tumor (80%) compared to the controls (21%); K II: 29%. All patients and patients with a K I tumor had a significant longer smoking career (39.3 years; 39.6 years) and a higher tar exposure (TE = 1767; TE - 1810) compared to the controls (31.9 years, TE = 1146). K II: 37.4 years, TE = 1508. Lung cancer risks (adj. for TE) and population attributable risks (PAR) were: all age groups R = 7.3*, PAR = 54%; less than 40 years R = 1.1, PAR = 3%; 41-50 years R = 4.2*, PAR = 42% ; 51-60 years R = 7.6*, PAR = 62%; 61-70 years R = 7.8*, PAR = 54%; greater than 71 years R = 8.0*, PAR = 55%. Lung cancer risks (adj. for age) in relation to tar exposure and attributable risks (AR) were: TE less than 500: all cases R = 1.5, AT = 34% (KIR = 2.9, K II R = 0.8); TE 501-1000: all cases R = 4.2*, AR = 76% (KIR = 9.9*, K II R - 1.1): TE 1001-2000: all cases R = 12.1*, AR = 92% (KIR = 27.2*, K II R = 2.6**); TE 2001-3000: all cases R = 11.1*, AR = 91% (KIR = 25.2*, K II R = 2.0); TE greater than 3001: all cases R = 13.0*, AR = 92% (KIR = 29.3*, K II R = 3.3). These is a significant increase of risk of cigarette smokers beyond a TE of 501, which could be identified as a sort of critical exposure. There is a pronounced dose response relationship between cigarette smoking in relation to TE and lung cancer risk as concerning K I tumors but not KII tumors. Lung cancer risks in relation to age began smoking: less than 19 years R = 7.8*; 19 years and above R = 6.5*. *P less than 1%, **P less than 5%.
对297名女性肺癌患者(克雷伯格I型:202例,克雷伯格II型:95例)和580名对照者的吸烟习惯进行了分析。此外,还计算了焦油暴露量(TE)。TE的计算包括所有曾吸食香烟品牌的消费量、持续时间和焦油含量。与对照者(21%)相比,患者(63%)及克雷伯格I型肿瘤患者(80%)中的吸烟者显著更多;克雷伯格II型为29%。与对照者(31.9年,TE = 1146)相比,所有患者及克雷伯格I型肿瘤患者的吸烟史显著更长(39.3年;39.6年),焦油暴露量更高(TE = 1767;TE = 1810)。克雷伯格II型:37.4年,TE = 1508。肺癌风险(校正TE)和人群归因风险(PAR)为:各年龄组R = 7.3*,PAR = 54%;小于40岁R = 1.1,PAR = 3%;41 - 50岁R = 4.2*,PAR = 42%;51 - 60岁R = 7.6*,PAR = 62%;61 - 70岁R = 7.8*,PAR = 54%;大于71岁R = 8.0*,PAR = 55%。与焦油暴露相关的肺癌风险(校正年龄)及归因风险(AR)为:TE小于500:所有病例R = 1.5,AR = 34%(克雷伯格I型R = 2.9,克雷伯格II型R = 0.8);TE 501 - 1000:所有病例R = 4.2*,AR = 76%(克雷伯格I型R = 9.9*,克雷伯格II型R = 1.1);TE 1001 - 2000:所有病例R = 12.1*,AR = 92%(克雷伯格I型R = 27.2*,克雷伯格II型R = 2.6**);TE 2001 - 3000:所有病例R = 11.1*,AR = 91%(克雷伯格I型R = 25.2*,克雷伯格II型R = 2.0);TE大于3001:所有病例R = 13.0*,AR = 92%(克雷伯格I型R = 29.3*,克雷伯格II型R = 3.3)。当TE超过501时,吸烟者的风险显著增加,这可被视为一种临界暴露。就克雷伯格I型肿瘤而言,吸烟与TE和肺癌风险之间存在明显的剂量反应关系,但克雷伯格II型肿瘤不存在。与开始吸烟年龄相关的肺癌风险:小于19岁R = 7.8*;19岁及以上R = 6.5*。*P小于1%,**P小于5%。