Fire fighters are exposed to irritating, asphyxiating, and toxic gases and aerosols, to psychological stress, and to physically demanding work. Due to differences in fire fighting techniques, exposure conditions for fire fighters differ among different countries. The purpose of this investigation was to study cancer incidence and mortality in fire fighters who have been working with fire fighting methods used in Sweden from the beginning of this century onwards. All male fire fighters employed for at least 1 year in the City of Stockholm during 1931-1983 were traced, and an index of the number of fires fought was calculated for each individual. The mortality during 1951-1986 (among 1, 116 fire fighters) was lower than expected (SMR = 82; 95% confidence interval 72-91) compared with local mortality rates, with a low mortality in circulatory diseases, obstructive lung diseases, violent deaths, and suicides. The cancer incidence in 1958-1986 was equal to the expected (SMR = 100; 95% confidence interval 83-119). However, an excess of stomach cancer (18 observed vs. 9.37 expected; SMR = 192, 95% CI 114-304) was observed. There was also a tendency for higher incidence and mortality in stomach and brain cancer with increasing number of fires. There were four deaths from brain cancer compared to 0.8 expected (SMR = 496; 95% CI 135-1270) in the highest exposure category. Fire fighters are, however, not systematically exposed to known stomach or brain carcinogens, and the results need confirmation in further studies with extensive exposure evaluations.

Thirty-six car painters and 115 control persons participated in a follow-up investigation 6 years after the initial study, including measurement of lung function (dynamic spirometry and nitrogen washout test) and estimation of exposure to diisocyanates based on individual working routines, use of respiratory protection equipment, and measurements. The mean exposure for the car painters was 0.0015 mg/m3 hexamethylenediisocyanate (HDI) and 0.09 mg/m3 hexamethylenediisocyanate-biurettrimer (HDI-BT), but frequently there were peak exposures exceeding 2.0 mg/m3 HDI-BT for at least 30 sec. Compared with smoking controls, the smoking car painters had greater yearly reduction in FVC (95 versus 38 ml), FEV1 (61 versus 28 ml), and VC (77 versus 30 ml). The nonsmoking car painters showed no differences in lung volumes compared with their nonsmoking controls. The impairment correlated well with the frequency of high peak exposures to HDI-BT, but not with the mean exposure to diisocyanates.

Objectives-To examine if car painters who work with polyurethane paints that contain hexamethylenediisocyanate (HDI) and hexamethylenediisocyanate biuret trimer (HDI-BT) develop acute as well as chronic impairment of lung function.Methods-In this study data were reanalysed from two earlier studies on a group of car painters to see if a decrease in lung function within the week is a marker of vulnerability in those workers.Data on changes in forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) within the week were available for 20 car painters who were also examined six years later. Results-10 men showed a decline in FVC within the week. There were no significant differences in age, duration of employment, exposures during the follow up period, or smoking between car painters who had decline in lung function within the week and car painters who had not. A significant correlation was found between the change in FVC within the week and the long term (six year) change in FVC, standardised for the effects of aging and smoking, and adjusted for the number of peak exposures. Conclusions-The results suggest that the decrease in FVC within the week might serve as a guide to identify car painters at risk of a further decrement in lung function above the effects of aging, smoking, and exposure. (Occup Environ Med 1995;52:192-195)

No abstract

A fire-fighter, who developed chronic severe asthma after exposure to decomposition products of plastics during routine fire-fighting, is described. The outcome was fatal 25 months after onset of the disease.