The incidence of pulmonary tuberculosis among pathology workers in Japan is elevated, presumably due to frequent exposure to tubercle bacilli in the work place. To demonstrate the etiological significance of the association between this disease and occupation epidemiologically, a questionnaire survey was performed to assess the incidence of pulmonary tuberculosis among 1,201 pathologists and 1,187 pathology technicians throughout Japan. Pathology department workers other than pathologists and technicians, such as secretaries (n = 207), and workers in university departments of preventive medicine and public health (n = 732) served as control groups. While non‐occupation‐related tuberculosis was found in both departmental groups with nearly equal incidence, the incidence of pulmonary tuberculosis among pathologists and pathology technicians after engagement in their current specialist work was significantly higher than that in the control groups (odds ratio = 6.08–10.98). The incidence of disease among pathology technicians who assisted in autopsies was markedly higher than among those not involved in autopsies (odds ratio = 6.65). This elevated incidence was significantly related to the duration of work in pathology activities, and showed little change over the last decade. These findings indicate that specific environmental conditions in pathology departments, particularly autopsy of cadavers harboring active tuberculosis, constitute a serious occupational hazard. Acta Pathol Jpn 40: 116–127, 1990.

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Establishment of an exposure-effect relationship was attempted between personal nitrogen dioxide (NO2) exposure and urinary hydroxyproline to creatinine ratio of approximately 800 adult women, who were mothers of primary schoolchildren living in two communities around Tokyo. Daily average of the personal NO2 exposure (ENO2) was measured during wintertime by a newly developed personal monitor exposed for 24 hours. The hydroxyproline to creatinine ratio (HOP:C) in the urine sample collected early in the morning of the day for ENO2 measurement was used as a biochemical indicator of the health effect of NO2 exposure. The HOP:C was found to have significant correlation with ENO2 and number of cigarettes smoked actively and passively. ENO2, however, had no correlation with the intensity of the smoking levels; they might affect HOP:C independently. Stepwise multiple regression analysis revealed that HOP:C could be predicted by ENO2 and smoking habits at a high confidence level. The regression analysis of the active smokers' group indicated that a few cigarettes was enough to increase the HOP:C, while in the case of passive smoking, HOP:C increased proportionally to the number of cigarettes.

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