OBJECTIVE: To describe the national trends in lung cancer incidence among young adults and the relationship to adolescent smoking. METHODS: Between 1954 and 1998, a total of 1108 non-carcinoid lung cancers were reported to the Cancer Registry of Norway in individuals aged 20-44 years. Temporal variations were studied in age and sex specific rates, in age-adjusted rates, and by means of age-period-cohort modelling. The association between cancer incidence and smoking prevalence was evaluated. RESULTS: The lung cancer incidence rate among women aged 40-44 in Norway continued to increase into the most recent time interval (1994-1998) whereas the rate among men aged 40-44 was essentially constant after 1970. Consequently, lung cancer incidence rates converged among male and female young adults. Lung cancer incidence rates at age 40-44 were highly correlated with smoking prevalence at age 15-19 in males ( r = 0.88) and females ( r = 0.82) within the same birth cohort. CONCLUSIONS: The lung cancer incidence rate in young Norwegian women now equals that of men. The risk at age 40-44 was closely associated with teenage smoking, indicating that duration and age of onset are important.
Occupational exposure to combustion products rich in polycyclic aromatic hydrocarbons and particles is associated with an increased risk of lung cancer. This study aimed to evaluate whether the risk depended on the age at which the individuals were exposed.
Data from 1042 lung cancer cases and 2364 frequency-matched population controls selected from all men aged 40-75 years residing in Stockholm County, Sweden, at any time between 1985 and 1990, included detailed questionnaire information on occupational, residential, and smoking history. Occupational exposures were assessed by an occupational hygienist, and exposure to air pollution from road traffic was estimated based on dispersion models.
We found that individuals exposed to combustion products in their twenties were at higher risk than those never exposed (adjusted OR = 1.46; 95% CI 1.02, 2.10). The association was still evident after adjusting for a number of potential confounders, including lifetime cumulative exposure and latency. No clear association was found in those exposed at older ages.
Exposure to combustion products at a young age was associated with elevated risk of lung cancer. Exposure-reduction programs should be aware of the susceptibility of the younger employees.
BACKGROUND: Air pollution is suspected to cause lung cancer. The purpose was to investigate whether the concentration of nitrogen oxides (NOx) at the residence, used as an indicator of air pollution from traffic, is associated with risk for lung cancer. METHODS: We identified 679 lung cancer cases in the Danish Cancer Registry from the members of three prospective cohorts and selected a comparison group of 3,481 persons from the same cohorts in a case-cohort design. Residential addresses from January 1, 1971, were traced in the Central Population Registry. The NOx concentration at each address was calculated by dispersion models, and the time-weighted average concentration for all addresses was calculated for each person. We used Cox models to estimate incidence rate ratios after adjustment for smoking (status, duration, and intensity), educational level, body mass index, and alcohol consumption. RESULTS: The incidence rate ratios for lung cancer were 1.30 [95% confidence interval (95% CI), 1.07-1.57] and 1.45 (95% CI, 1.12-1.88) for NOx concentrations of 30 to 72 and >72 microg/m3, respectively, when compared with
The epidemiological evidence relating alcohol consumption and lung cancer is reviewed. Four correlation studies have shown a relationship between alcohol, particularly beer, consumption and lung cancer. Beer consumption was a risk factor in one case-control study. Eight out of ten prospective studies show alcoholics and high alcohol consumers to be at greater risk of lung cancer. Not all of the increased risk in these studies is explainable in terms of confounding by tobacco consumption. There is some animal evidence which supports the effects of alcohol on the likelihood of developing lung cancer.
Alcohol consumption has been associated with an increased risk of lung cancer, but the antioxidants in wine may, in theory, provide protection. This association was studied in 28,160 men and women subjects from three prospective studies conducted in 1964-1992 in Copenhagen, Denmark. After adjustment for age, smoking, and education, a low to moderate alcohol intake (1-20 drinks per week) was not associated with an increased risk of lung cancer. Men who consumed 21-41 and more than 41 drinks per week had relative risks of 1.23 (95% confidence interval (CI) 0.88-1.74) and 1.57 (95% CI 1.06-2.33), respectively. The risk of lung cancer differed according to the type of alcohol consumed: After abstainers were excluded, drinkers of 1-13 and more than 13 glasses of wine per week had relative risks of 0.78 (95% CI 0.63-0.97) and 0.44 (95% CI 0.22-0.86), respectively, as compared with nondrinkers of wine (p for trend = 0.002). Corresponding relative risks for beer intake were 1.09 (95% CI 0.83-1.43) and 1.36 (95% CI 1.02-1.82), respectively (p for trend = 0.01); for spirits, they were 1.21 (95% CI 0.97-1.50) and 1.46 (95% CI 0.99-2.14), respectively (p for trend = 0.02). In women, the ability to detect associations with high alcohol intake and type of beverage was limited because of a limited range of alcohol intake. The authors concluded that in men, a high consumption of beer and spirits is associated with an increased risk of lung cancer, whereas wine intake may protect against the development of lung cancer.
The incidence of cancer was studied in a population-based cohort of 9,353 individuals (8,340 men and 1,013 women) with a discharge diagnosis of alcoholism in 1965-83, followed up for 19 years (mean 7.7). After exclusion of cancers in the first year of follow-up, 491 cancers were observed cf 343.2 expected through 1984 (standardized incidence ratio [SIR] = 1.4, 95 percent confidence interval [CI] = 1.3-1.6). A similar excess risk of cancer was seen among men (SIR = 1.4, CI = 1.3-1.6) and among women (SIR = 1.5, CI = 1.1-2.0). We observed the established associations with cancers of the oral cavity and pharynx (SIR = 4.1, CI = 2.9-5.7), esophagus (SIR = 6.8, CI = 4.5-9.9), larynx (SIR = 3.3, CI = 1.7-6.0), and lung (SIR = 2.1, CI = 1.7-2.6), although confounding by smoking likely increased these risk estimates. While there was evidence of increased risk for pancreatic cancer (SIR = 1.5, CI = 0.9-2.3), alcoholism did not elevate the incidence of cancer of the stomach (SIR = 0.9, CI = 6-1.4), large bowel (SIR = 1.1, CI = 0.8-1.5), prostate (SIR = 1.0, CI = 0.8-1.3), urinary bladder (SIR = 1.0, CI = 0.6-1.5), or of malignant melanoma (SIR = 0.9, CI = 0.3-1.9). Among women, the number of breast cancers observed was close to expected (SIR = 1.2, CI = 0.6-2.2), although a significant excess number of cervical cancers occurred (SIR = 4.2, CI = 1.5-9.1).(ABSTRACT TRUNCATED AT 250 WORDS)
The U.S. National Cancer Institute and the Finnish National Public Institute jointly sponsored a large double-blind, placebo-controlled primary-prevention trial to examine the effects of vitamin E and beta-carotene supplementation on reducing the incidence of lung cancers in male smokers, ages 50-69 years. Supplementation did not result in a significant reduction in lung cancer, and a higher incidence of lung cancer was observed in the group receiving beta-carotene. These results should be examined within the context of the population studied before they are cited as definitive.
The study was devoted to the evaluation of technogenic geochemical pollution of the residential area of an industrial town and its effects on lung cancer incidence in the population living under severe exposure to emissions of a copper smelter plant. For mathematical treatment of epidemiologic data there were used methods of a system multifactor analysis based on pattern recognition principles. The result of the long-term operation of the copper smelter plant was established to become the intensive technogenic pollution of environment with carcinogenic substances. The contribution of environmental contamination in the lung cancer incidence of the population exposed to industrial emissions of the copper smelter was shown to be about 10%.
Analysts of epidemiologic data often contend with the problem of estimating the independent effects of many correlated exposures. General approaches include assessing each exposure separately, adjusting for some subset of other exposures, or assessing all exposures simultaneously in a single model such as semi-Bayes modeling. The optimal strategy remains uncertain, and it is unclear to what extent different reasonable approaches influence findings. We provide an empirical comparison of results from several modeling strategies.
In an occupational case-control study of lung cancer with 184 exposure substances, we implemented 6 modeling strategies to estimate odds ratios for each exposure-cancer association. These included one-exposure-at-a-time models with various confounder selection criteria (such as a priori selection or a change-in-the-estimate criterion) and semi-Bayes models, one version of which integrated information on previous evidence and chemical properties.
While distributions of odds ratios were broadly similar across the 6 analytic strategies, there were some differences in point estimates and in substances manifesting statistically significant odds ratios, particularly between strategies with few or no occupational covariates and those with many. Semi-Bayes models produced fewer statistically significant odds ratios than other methods. A simple semi-Bayes model that shrank all the 184 estimates to a common mean yielded nearly identical results to one that integrated considerable prior information.
Different modeling strategies can lead to different results. Considering the conceptual and pragmatic difficulties of identifying confounders, these results suggest that it would be unwise to place uncritical reliance on any single strategy.