The epidemic of respiratory cancer in the town of Armadale: The use of long-term epidemiological...
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s2 On air pollution, environmental tobacco smoke, radon, and lung cancer. Crawford WA. Occupational and Environmental Health Consultancy, Seaforfh, NSW 2992. J Air Pollut Control Assoc 198838: 1386-91. The health of populations in industrialised societies has been affected for many years by ambient air pollutants presenting a threat of chronic bmnchitisandlungcancer.Inthe 1980sindoorpollutantsreceivedmuch needed investigation to assess their hazards to health. Exposure to environmental tobacco smoke and radon is now the subject of much research and concern. This review attempts to put some perspective on lung cancer that is attributable to lifetime exposure to airborne pollut- ants. The view is expressed that air pollution control authorities have played and are playing a major role in health improvement. The epidemic of respiratory cancer in the town of Armadale: The use of long-term epidemiological surveillance to test a causal hy- pothesis. Williams FLR, Lloyd OL. Environmental Epidemiology and Cancer Ceture, Department of Community Medicine, Ninewells Medical School, UniversityofDundee, Dundee. Public Health 1988;102:531-8. In 1978, a geographical association was reported between air pollu- tion from a steel foundry and high mortality from lung cancer in the adjacentresidentialareaofthe townofArmadale,Scotland.Subsequent studies validated the mortality findings for lung cancer, demonstrated other epidemiological abnormalities, and examined the detailed pat- terns of environmental pollution. We summarise these findings and also report the outcome of the follow-up surveillance which demonstrated the end of the epidemic of lung cancer, both in the town as a whole and in the ‘at risk’ area. The sequence of epidemiological, environmental and industrial events was consistent with the hypothesis that air pollu- tion fmm a steel foundry was causally linked with the short-latency epidemic of lung cancer in the town. Indoor radon exposure and active and passive smoking in relation to the occurrence of lung cancer. Axelson 0, Andersson K, Desai G et al. Department of Occupational Medicine, University Hospiral. 58185 Linkaping. Stand J Work Envi- ron Health 1988;14:286-92. Exposure to indoor radon and radon daughters is currently attracting great interest as a possible cause of lung cancer. This concern is supported by several studies, most of them relatively small in numbers or weak in the assessment of exposure. This study encompasses 177 persons with lung cancer and 677 noncancer referents, all deceased and with 30 years or more of residency in the same house in an area with radon-leaking ahtm shale deposits in the central part of southern Sweden. Exposure categories based on building material, type of house, and ground conditions were created, but measurements of the indoor radon daughter concentration were also made for 142 cases and 264 referents. Active and passive smoking was ascertained through ques- tionnaires sent to the next-of-kin. Overall, the lung cancer risk was approximately twofold with regard to the categories of assumed radon daughter exposure for the rural sector of the population but not for the same categories of the urban sector, possibly because of less precise exposure assessment and influence from other factors. Occasional and passive smokers, as well as passive smokers alone, had a particularly increased risk of lung cancer in association with the increased exposure categories. Fifty-year trend in incidence rates of bronchogenic carcinoma by cell type in Olmsted County, Minnesota. Beard CM, Jedd MB, Woolner LB, Richardson RL, Bergstralh EJ, Melton L.J. III. Department ofHealth Sciences Research, Mayo Clinic and Foundakon, Rochester, MN 55905. J Natl Cancer Inst 1988;80:1404-7. An earlier report suggested that incidence rates of primary bmncho- genie carcinoma had leveled off for men in Olmsted County, MN. Extension of that study to cover 50 years in this midwestem community now shows that lung cancer incidence continues to increase in both sexes,withrates in womenapproachingthosefoundinmen20yearsago. This increase was seen for all cell types of bmnchogenic carcinoma. Because one pathologist reevaluated tissues, changing histologic clas- sifications were not responsible for secular trends; now were the results influenced by referral bias inasmuch as the study was population based. Cancers of the respiratory tract in mustard gas workers. Easton DF, Peto I, Doll R. Section ofEpidemiology. Institute ofcancer Research, Sutton, Surrey SM2 5 PX. Br J Ind Med 1988;45:652-9. In a study of a cohort of 2498 men and 1032 women employed in the manufacture of mustard gas in Cheshire during the second world war 3354 (95%) individuals were successfully traced for mortality to the end of 1984. Large and highly significant excesses were observed as compared with national death rates for deaths from cancer of the larynx (11 deaths observed, 4.04 expected, p = 0.003). pharynx (15 observed, 2.73 expected, p c O.OOl), and all other buccal cavity and upper respiratory sitescombined (lip, tongue, salivary gland, mouth,nose) (12 observed,4.29expected,p=0.002).Forlungcancer,ahighlysignificant but more moderate excess was observed (200 observed, 138.39 ex- pected, p < 0.001). Significant excesses were also observed for deaths from acute and chronic non-malignant respiratory disease (131 ob- served, 91.87 expected and 185 observed, 116.31 expected, respec- tively). The risks for cancers of the pharynx and lung were significantly related to duration of employment. None of these results is substantially altered when expected numbers are calculated from Cheshire urban areas rather than national rates, although the relative risks for lung cancer and non-malignant respiratory disease are substantially reduced if rates for Merseyside, the nearest large conurbation, are used. The results provide strong evidence that exposure to mustard gas can cause cancers of the upper respiratory tract and some evidence that itcan cause lung cancer and non-malignant respiratory disease. Significant excess mortality wasalsoobservedforcancersoftheoesophagus(20observed, 10.72 expected) and stomach (70 observed, 49.57 expected) but these excesses showed no consistent relation with time since first exposure or duration of exposure, and it is not clear whether they were caused by mustard gas or were due to a combination of chance and confounding. Air pollution and lung cancer mortality in Harris County, Texas, 1979-1981. Buffler PA, Cooper SP, Stinnett S, Contant C, Shirts S, Hardy RJ, Agu V,Gehan B, Burau K. Epidemiology Research Unit, UniversityofTexas Health Science Center. School of Public Health, Houston TX 77225. Am J Epidemiol 1988;128:683-99. Elevated lung cancer mortality rates in Harris County, Texas com- pared with other US counties and previously published reports that suggested a causal relation between air pollution and lung cancer in Houston prompted this ecologic analysis. A weighted regression analy- sis was used to examine the air pollution-lung cancer mortality relation for white males in Harris County, Texas, 1979-1981. The regression model included the following census tract-specific characteristics: median age for white males, two social and demographic factors not strongly correlated with pollution (family life cycle and migration), an age-dependent smoking index, and a pollution measure based on total suspended particulates. This model indicated a statistically significant contribution of the pollution measure in explaining the intracounty variation in lung cancer mortality rates. The relation between air pollution and lung cancer mortality, however, appeared to be highly dependent on which social and demographic factors were selected for inclusion in the analysis. Air pollution was not demonstrated to be a strong determinant of lung cancer mortality in this study in that the
Transcript of The epidemic of respiratory cancer in the town of Armadale: The use of long-term epidemiological...
s2
On air pollution, environmental tobacco smoke, radon, and lung cancer. Crawford WA. Occupational and Environmental Health Consultancy, Seaforfh, NSW 2992. J Air Pollut Control Assoc 198838: 1386-91.
The health of populations in industrialised societies has been affected for many years by ambient air pollutants presenting a threat of chronic bmnchitisandlungcancer.Inthe 1980sindoorpollutantsreceivedmuch needed investigation to assess their hazards to health. Exposure to environmental tobacco smoke and radon is now the subject of much research and concern. This review attempts to put some perspective on lung cancer that is attributable to lifetime exposure to airborne pollut- ants. The view is expressed that air pollution control authorities have played and are playing a major role in health improvement.
The epidemic of respiratory cancer in the town of Armadale: The use of long-term epidemiological surveillance to test a causal hy- pothesis. Williams FLR, Lloyd OL. Environmental Epidemiology and Cancer Ceture, Department of Community Medicine, Ninewells Medical School, UniversityofDundee, Dundee. Public Health 1988;102:531-8.
In 1978, a geographical association was reported between air pollu- tion from a steel foundry and high mortality from lung cancer in the adjacentresidentialareaofthe townofArmadale,Scotland.Subsequent studies validated the mortality findings for lung cancer, demonstrated other epidemiological abnormalities, and examined the detailed pat- terns of environmental pollution. We summarise these findings and also report the outcome of the follow-up surveillance which demonstrated the end of the epidemic of lung cancer, both in the town as a whole and in the ‘at risk’ area. The sequence of epidemiological, environmental and industrial events was consistent with the hypothesis that air pollu- tion fmm a steel foundry was causally linked with the short-latency epidemic of lung cancer in the town.
Indoor radon exposure and active and passive smoking in relation to the occurrence of lung cancer. Axelson 0, Andersson K, Desai G et al. Department of Occupational Medicine, University Hospiral. 58185 Linkaping. Stand J Work Envi- ron Health 1988;14:286-92.
Exposure to indoor radon and radon daughters is currently attracting great interest as a possible cause of lung cancer. This concern is supported by several studies, most of them relatively small in numbers or weak in the assessment of exposure. This study encompasses 177 persons with lung cancer and 677 noncancer referents, all deceased and with 30 years or more of residency in the same house in an area with radon-leaking ahtm shale deposits in the central part of southern Sweden. Exposure categories based on building material, type of house, and ground conditions were created, but measurements of the indoor radon daughter concentration were also made for 142 cases and 264 referents. Active and passive smoking was ascertained through ques- tionnaires sent to the next-of-kin. Overall, the lung cancer risk was approximately twofold with regard to the categories of assumed radon daughter exposure for the rural sector of the population but not for the same categories of the urban sector, possibly because of less precise exposure assessment and influence from other factors. Occasional and passive smokers, as well as passive smokers alone, had a particularly increased risk of lung cancer in association with the increased exposure categories.
Fifty-year trend in incidence rates of bronchogenic carcinoma by cell type in Olmsted County, Minnesota. Beard CM, Jedd MB, Woolner LB, Richardson RL, Bergstralh EJ, Melton L.J. III. Department ofHealth Sciences Research, Mayo Clinic and Foundakon, Rochester, MN 55905. J Natl Cancer Inst 1988;80:1404-7.
An earlier report suggested that incidence rates of primary bmncho- genie carcinoma had leveled off for men in Olmsted County, MN. Extension of that study to cover 50 years in this midwestem community now shows that lung cancer incidence continues to increase in both sexes,withrates in womenapproachingthosefoundinmen20yearsago. This increase was seen for all cell types of bmnchogenic carcinoma. Because one pathologist reevaluated tissues, changing histologic clas- sifications were not responsible for secular trends; now were the results influenced by referral bias inasmuch as the study was population based.
Cancers of the respiratory tract in mustard gas workers. Easton DF, Peto I, Doll R. Section ofEpidemiology. Institute ofcancer Research, Sutton, Surrey SM2 5 PX. Br J Ind Med 1988;45:652-9.
In a study of a cohort of 2498 men and 1032 women employed in the manufacture of mustard gas in Cheshire during the second world war 3354 (95%) individuals were successfully traced for mortality to the end of 1984. Large and highly significant excesses were observed as compared with national death rates for deaths from cancer of the larynx (11 deaths observed, 4.04 expected, p = 0.003). pharynx (15 observed, 2.73 expected, p c O.OOl), and all other buccal cavity and upper respiratory sitescombined (lip, tongue, salivary gland, mouth,nose) (12 observed,4.29expected,p=0.002).Forlungcancer,ahighlysignificant but more moderate excess was observed (200 observed, 138.39 ex- pected, p < 0.001). Significant excesses were also observed for deaths from acute and chronic non-malignant respiratory disease (131 ob- served, 91.87 expected and 185 observed, 116.31 expected, respec- tively). The risks for cancers of the pharynx and lung were significantly related to duration of employment. None of these results is substantially altered when expected numbers are calculated from Cheshire urban areas rather than national rates, although the relative risks for lung cancer and non-malignant respiratory disease are substantially reduced if rates for Merseyside, the nearest large conurbation, are used. The results provide strong evidence that exposure to mustard gas can cause cancers of the upper respiratory tract and some evidence that itcan cause lung cancer and non-malignant respiratory disease. Significant excess mortality wasalsoobservedforcancersoftheoesophagus(20observed, 10.72 expected) and stomach (70 observed, 49.57 expected) but these excesses showed no consistent relation with time since first exposure or duration of exposure, and it is not clear whether they were caused by mustard gas or were due to a combination of chance and confounding.
Air pollution and lung cancer mortality in Harris County, Texas, 1979-1981. Buffler PA, Cooper SP, Stinnett S, Contant C, Shirts S, Hardy RJ, Agu V,Gehan B, Burau K. Epidemiology Research Unit, UniversityofTexas Health Science Center. School of Public Health, Houston TX 77225. Am J Epidemiol 1988;128:683-99.
Elevated lung cancer mortality rates in Harris County, Texas com- pared with other US counties and previously published reports that suggested a causal relation between air pollution and lung cancer in Houston prompted this ecologic analysis. A weighted regression analy- sis was used to examine the air pollution-lung cancer mortality relation for white males in Harris County, Texas, 1979-1981. The regression model included the following census tract-specific characteristics: median age for white males, two social and demographic factors not strongly correlated with pollution (family life cycle and migration), an age-dependent smoking index, and a pollution measure based on total suspended particulates. This model indicated a statistically significant contribution of the pollution measure in explaining the intracounty variation in lung cancer mortality rates. The relation between air pollution and lung cancer mortality, however, appeared to be highly dependent on which social and demographic factors were selected for inclusion in the analysis. Air pollution was not demonstrated to be a strong determinant of lung cancer mortality in this study in that the
