Lung Cuncer. 7 (I 991) 261-278 Elsewer

261

ABSTRACTS

Prevention

Use of “time windows” to investigate lung cancer latency intervals at an Ontario steel plant Finkelstein MM. Heolrh Studies Service. Onfario Mimstry of Lobour.

400 Universiry Avenue, 8rh Floor, Ibronto, Onr., M7A 177. Am J Ind Med 1991;19:229-35.

This paper describes an apphcation of the time wmdows method to an examination of the temporal pattern of lung cancer risk among steel workers. Case-control methodology was utilized. The cases were 36 men who had died of lung cancer and the controls were 289 men who had died of any other cause. The number of years ol employment in the steel pouringareawasusedasasurrogatemeasureofexposure. Thedata wereexaminedbycontingency tableanalysisandbylogistic regression, which permitted adjustment for exposures in multiple time windows and the use of continuous, rather than categorical, measures of expo- sure. II was found that lung cancer risk was associated with exposures occurring between 18 and 30 years before death. It cannot yet be determined whether this time course reflects a biological response or the temporal pattern of exposure to an as yet unidentified toxic agent.

Screening for lung cancer. A critique of the Mayo Lung Project Fontana RS, Sandcrson DR. Woolner LB, Taylor WF, Miller WE, Muhm JR et al. Division of Thoracic Diseases and internal Medrcme,

DeparrmentofDiagnoslic Radiology. MayoClinic. ZWFirslSlreer SW,

Rochester, MN55905. Cancer 1991;67:Suppl 1155-64. The National Cancer Institute of the United States recently sponsored

three large-scale. randomized controlled trials of screening for early lung cancer. The trials were conducted at the Johns Hopkins Medical Institutions, the Memorial Sloan Kettering Cancer Center, and the Mayo Clinic. Participants were middle-aged and older men who were chronic heavycigarettesmokcrsand thusathighriskofdevelopinghmg cancer. Screening procedures were chest radiography and sputum cytology, the only screening tests of established value for detecting early stage, asymptomatic lung cancer. In the Hopkins and Memorial trials the study population was offered yearly chest radiography plus sputum cytology every 4 months, The control population was offered yearly chest radiography only. In these trials the addition of sputum cytology appeared to confer no lung cancer mortality rate advantage. The Mayo Clinic trial compared offering chest radiography and sputum cylologyevery4 monthstoofferingadvice that the twotestsbeobtained once a year. This trial demonstrated stgnificantly increased lung cancer detection, resectability,and survivorship in the group offered screening every 4 months compared with the control group. However, there was no significant ditTcrence in lung cancer mortality rate between the two groups. The statistical power of these trials was somewhat limited. Nevcrthclcss, results do not justify rccommendmg large-scale radiol- ogic or cytologic screening for early lung cancer at this time.

Epidemiology and etiology

hIcreased risk of lung cancer in the melting department of a second Ontario steel manufacturer Finkelstein MM, Boulard M, Wilk N. Health Sudies Service, Ontario

Ministry of Labour, 400 University Avenue. 8th Floor. Toronto, Ont.,

M7A 1T7. Am J Ind Med 1991;19:183-94. A study of lung cancer among workers at an electric arc steel making

operation was performed to follow up on the observation of a lung cancer cluster in the melt shop of another plant. The study group comprised 335 deceased men identified from plant records. Eight of thirty men who had ever worked in the pouring pit area died of lung cancer(PMR 276; p < 0.01). but increased risk was not found elsewhere in the melting department. There was a significant trend in lung cancer risk with the length of employment tn the pit area during a time window 18-30 years before death. Smoking data suggested that smoking alone could not account for the increased risk. An industrial hygiene assess-

ment found present exposures to carcinogenic metals and sihca to be within current guidelines. No polycyclic aromatic hydrocarbons were detected. This is the second steel plant for which we have found increased lung cancer risk in the pouring areas. The causative factors have not yet been identified.

Crystalline silica and lung cancer: A review of recent experimental evidence Holland LM. He&h, Safely and Environment Division, Los Alamos

National Laboratory. MS K499, Box 1663, Los Alamos. NM 87545.

Regul Toxicol Pharmacol 1990;12:224-37. The International Agency for Research in Cancer (IARC) has re-

cently staled that crystalline sihca should be regarded as a potential carcinogen. The IARC bases this statement on a Ending that there is limited evidence of carcinogenicity in humans and sufficient evidence for carcinogenicity in animals. Recent laboratory animal experiments demonstrating a carcinogenic response to silica exposure have intensi- lied scienttfic and regulatory concern lor crystalline silica as a respira- tory carcinogen. Studiesof human populations have been contradictory in demonstrating a causal relationship between crystalline silica expo sure and lung cancer. This paper reviews recent experimental evidence and attempts to identify the gaps and inconsistencies in our understand- ing of the relationship between exposure to crystalline sdrca and the 1~0 diseases of concern: silicosis and pulmonary neoplasia. Given our current level of understanding and the need for more sctenliftc data it seemspremature to initiatechanges in cxposureregulationsatthislime.

Potential lung cancer risk from indoor radon exposure Harley NH, Harley IH. Institute of Environmental Medicme. New York

University Medical Center. New York, NY. CA Cancer J Chn 1990$0%5- 75.

The contribution of radon daughter exposure to excess lung cancer in underground mtners is universally accepted. These mmers received exposures from tens to thousands of WLM in a relatively few years. Although the miners were also exposed to other noxious agents in mines, the appearance of the excess lung cancer mortality in several types of mines and the mcrease with increasing exposure provtde convincing evidence of the role of radon as the carcinogen. It IS conceivable that exposures to radon at an average concentration of one to two pCi/Iiler. the levels for a majority of homes, might not produce cxccss lung cancers. This would require that a lifettme exposure at low concentrations produce a different response from that of a few years al higher levels for the miners. This is unlikely but not impossible. The current environmental epidemiology is of varying quality. The better studies may give some answers in a few years. These studies are more likely to establish an upper limit of risk than to provide an exposure- response model. Present risk estimates cannot be used accurately in es- ttmating the overall lung cancer rtsk to the US population, since there are no good data on average exposure and exposure distribution. For example, the number of homes above the EPA gutdeline of four pCi/ liter may range from two million to IOmillion. Anestimateof theactual radon exposure in the US may be forthcoming from a planned EPA survey. But these data will not be available for a few years. In the conservative tradition of radiation protection, indoor radon exposures in homes are estimated to produce a number of excess lung cancers m the population. One estimate by the NCRP’ is about 10,OCQ deaths per year in the US, for an average annual estimated exposure of 0.2 WLM (about one pCi/Iiter). The National Academy of Sciences (BEIR IV)” estimates 13,tXkl deaths for the same exposure, and the EPA’s estimate is 5,ooo to 20, ooo.

Specific Ki-rascodon61 mutations may determine thedevelopment of urethan-induced mouse lung adenomas or adenocarcinomas Nuzum EO. Malkinson AM, Beer DC. Deparmtent of Pharmacology,

Toxicology and Therapeutics, University of Kansas Medical Center.

39th and Rambow Boulevard. Kansas City. KS 66103. Mol Carclnog

1990:3:287-95.

In A/J strain mice, the carcinogen urethan induces lung adenomas and adenwarcinomas that contain Ki-ras-activating mutations primar- ily in codon 61. These mutationsaffect the middleadenine in codon 61