Smoking Lead-Exposed
and Blood Lead Concentrations in Workers and an Unexposed Population S. TOLA
AND C. H. NORDMAN
Received
April
30. 1976
Blood lead (Pb-B) concentrations were measured and the smoking history was taken from 355 men representing the general population and 2209 men occupationally exposed to lead. No association between smoking and Pb-B could be demonstrated in the men from the general population, but a dose-response relationship was found between the amount of smoking and the Pb-B concentrations of men occupationally exposed to lead. Smokers had statistically significantly higher Pb-B levels than nonsmokers. This result can probably be attributed to the contamination of fingers and cigarettes in the lead-exposed workplaces rather than to the small amount of lead contained in the cigarettes. The deleterious effect of smoking upon the lung clearance mechanism can also be a contributing factor.
INTRODUCTION
Smoking has been claimed to be associated causally with the higher blood lead (Pb-B) levels found in smokers as compared to nonsmokers (Hofreuter et al., 1961; Tepper and Levin, 1972). On the other hand, some recent studies have failed to demonstrate a difference between the two groups (Daines et nl., 1972; Lehnert et ~1.. 1967; McLaughlin and Stopps, 1973; Nordman, 1975; Thomas rt cl/. , 1967). All these reports have dealt with people without any known occupational lead exposure. In a survey of the Pb-B levels among the general Finnish population (Nordman, 1975) and one of workers occupationally exposed to lead (Tola et ctl., 1976), information was also collected on smoking habits. In the present investigation we have used the data of both surveys to study the association between the smoking and the Pb-B concentrations of men with different degrees of occupational lead exposure. MATERIAL
Between 1970 and 1973 a survey on the lead exposure of the general population was made by one of us (Nordman, 1975). From this material all men (N = 355) with accurately recorded smoking histories and no occupational or related exposure to lead were selected for the present study. Their mean age was 37 (SD 13) years. At the time of the survey on the genera1 population, 2209 workers occupationally exposed to lead in 30 different types of work were also studied (Tola rt al., 1976). Accurate information with regard to smoking habits was available for 2108 men, whose mean age was 36 (SD 12) years. From both the genera1 population and lead exposed workers, only those who either smoked cigarettes, were nonsmokers, or had stopped smoking were included. Those reporting pipe or cigar smoking were excluded because the group was small and also too heterogeneous with regard to smoking habits.
METHODS
The Pb-B concentrations were measured by the atomic absorption spectrophotometric method described by Hessel(l968). The method error for determinations from duplicate samples was 2.1 &IO0 ml. The intra- and interlaboratory method control has been described earlier (Nordman, 1975; Tola, 1973). Smoking histories were collected with a self-administered questionnaire. The following smoking categories were used: (1) has never smoked, (2) has smoked previously but has stopped smoking, (3) smokes l-20 cigarettes daily, (4) smokes more than 20 cigarettes daily, (5) smokes a pipe or cigars. Category 5 was excluded from the analyses. Since a more common occurrence of heavy lead exposure among the heavier smokers could bias the results, the material was arbitrarily stratified into three lead exposed groups, i.e., heavy, moderate, and slight. Previous experience determined the stratification in terms of types of work. For example, workers in storage battery manufacturing and shipbreaking were considered as heavily exposed, those in foundries and ammunition factories were considered moderately exposed, and those working in service stations and electric bulb factories were considered slightly exposed. In addition to exposure stratification the workers were also grouped by age: ~34, 35-49, and 150 years. RESULTS
Table I shows the means and standard deviations of the blood lead concentrations of the men from the general population and Table 2 presents those from the lead exposed workers. There were no statistically significant differences between the different smoking categories in the general population, but the difference between occupationally exposed smokers and nonsmokers was statistically significant. Moreover, Pb-B values tended to increase concomitantly with more smoking. These differences were statistically significant also in the age groups of ~34 years and 3.5-46 years. In the eldest age group the Pb-B values of the smokers were higher (mean 26.9) than those of the nonsmokers (mean 23.8), but this difference was not statistically significant. The Pb-B concentrations of the different occupationally exposed strata are shown in Tables 3-5. In each stratum the Pb-B concentrations of smokers were
Blood Smoking
category
Cigarettes daily 321 I - ‘0 Stopped smoking Never smoked o Calculations
were
performed
!V
Mean
30 131 49 135
10.8 11.4 10.8 10.1
after
logarithmic
lead concentration
transformation.
Mean
+ SD
14.8 16.2 15.9 14.4
(&I00
ml) Mean
- SD
7.9 x.1 7.3 7.2
252
TOLA
AND
NORDMAN
Blood Smoking
category
Cigarettes daily 321 1 - 20 Stopped smoking Never smoked (i Calculations
were
performed
N
Mean
296 947 355 537
30.1 28.5 25.9 24.4
after logarithmic
lead concentration Mean
(&IO0
+ SD
ml) Mean
51.3 48.1 42.5 40.3
transformation.
~ SD
17.6 16.8 15.8 14.8
F = 13.40. & = 3; 2104. P < 0.001.
statistically significantly higher than those of nonsmokers, and also the trend of higher Pb-B values with more smoking was evident. Both this trend and the statistically significant differences between smokers and nonsmokers could be demonstrated also in the age groups of s34 years and 3549 years. In the eldest age group statistical significance was not achieved although the trend of increasing Pb-B values with increasing smoking within different exposure strata was observed also for this age group. DISCUSSION
In our study the Pb-B levels of the general population revealed no differences between smokers and nonsmokers. This result coincides with the results of several recent studies (Daines et crl., 1972; Jones ef al., 1972; Lehnert et al., 1967; McLaughlin and Stopps, 1973; Nordman, 1975; Thomas et al., 1967). Other investigators have, however, claimed that smokers do have higher Pb-B levels than nonsmokers (Hofreuterrt al., 1961; Tepperand Levin, 1972; U.S. Dept. of Health, Education and Welfare, 1975). The elevated Pb-B levels of smokers without occupational lead exposure have been attributed to the small amounts of lead in tobacco leaves because of the former use of leaded pesticides (Cogbill and Hopps, 1957). Szadkowski and his colleagues (1969) determined that 3.1 pugis the average daily amount of lead absorbed from cigarette smoke for an average smoker (17 TABLE BLOOD
LEAD EXPOSED
CONCENTRA TO Lt.4~
3
I 10~s (/&lo0 ml) OF WORKERS HEAVILY AFFORDING ‘I’O SMOKING C.~ITSXIR~”
Blood Smoking
category
Cigarettes daily 321 1 - 20 Stopped smoking Never smoked 0 Calculations
were
performed
N
Mean
50 198 54 74
55.8 47.7 43.8 38.4
after
logarithmic
lead concentration Mean
+ SD
(&IO0
ml) Mean
88.5 78.6 78.1 65.5 transformation.
F = 5.93.
- SD
35.2 28.9 24.6 22.5 & = 3;372.
P < 0.001.
253
Blood Smoking
category
Cigarettes daily 321 I ~ 70 Stopped smoking Never smoked ” Calculations
were
performed
N
Mean
I74 419 701 313
29.1 26.3 ‘5.1 24.6
after logarithmic
lead concentration Mean
+ SD
(pg/lOO
ml) Mean
43.9 40.0 37. I 37.9
transformation.
- SD
19.3 17.3 17.0 15.9
F = 28.33. c(t‘ = 3;1 114. P < 0.001.
cigarettes/day). This amount is small in comparison with that absorbed daily from food, even though that absorbed from food displays a large individual and day-today variance (Nordman, 1975), and in comparison with the amount absorbed from air. Therefore, it seems questionable whether such a small amount would be reflected in the Pb-B level. Nevertheless, the contribution of lead from smoking to the daily lead absorption of the genera1 population can scarcely be regarded as hazardous to man’s health. Smoking in lead-exposed work environments seems to cause elevated Pb-B levels in smokers as compared to nonsmokers. Moreover, our results indicate a dose-response relationship between smoking and Pb-B concentrations. Although such a relationship was not statistically significant in the oldest age group of our study, a difference did exist between the Pb-B levels of smokers and nonsmokers. Thus the results within this group were considered consistent with the hypothesis of a causal association. The lead exposure provided by smoking among lead-exposed workers is different from that of the general population. The contamination of cigarettes and fingers with lead particles probably affects exposure more than the lead content of the cigarette itself. This effect seems to be more pronounced in the most exposed occupations; however, the wider range of the Pb-B values determined in this group contributed to the greater differences found within the group. Part of the effect of smoking on lead absorption in workers exposed to lead may
Smoking
category
Cigarettes daily 230 1 ~ 20 Stopped smoking Never smoked a Calculations
were
performed
N
Mean
95 170 99 150
2.7 31.5 20.7 19.3
after
logarithmic
transformation,
Mean
+ SD
Mean
14.6 14.2 13.5 12.2
35.2 35.6 31.8 30.8 F = 4.46. #
- SD
= 3:6)0.
p < 0.01.
254
TOLA
AND
NORDMAN
be explained by an impairment of the lung defense mechanisms, The inhalation of cigarette smoke is known to depress ciliary activity and the transportation of mucus in a variety of mammalian species (Dahlman, 1966). There is also evidence indicating that the length of cilia is decreased and the percentage of ciliated cells is diminished in human smokers (Ide et al., 1959). Moreover, Warr et a/. (1975) have recently reported that the alveolar macrophages of young smokers display a decreased phagocytic capacity. In addition lead has repeatedly been shown to decrease the number of alveolar macrophages in animals distinctly and thereby impair lung clearance (Bingham et al., 1968; Bruch et al., 1974). Theoretically, the combined effect of smoking and lead exposure on alveolar macrophages should be more severe than that of lead exposure alone. The importance of this combined effect remains to be assessed. Nevertheless, the effect of smoking on lung defense mechanisms is deleterious and is likely to cause an increase in the retention of such inhaled substances as lead particles in inhaled air and cigarette smoke. Our findings indicate a dose-response relationship between the smoking of occupationally exposed workers and elevated Pb-B levels. Because one possible source of the exposure is the environmental contamination offingers and cigarettes, personal hygiene ought to be emphasized and smoking in workrooms must be prohibited. Of course the ultimate solution would be for workers to stop smoking completely. ACKNOWLEDGMENTS We wish to thank Raili Vilhunen, M.Sc. (eng.), for the supervision of the laboratory analyses, Sisko Asp, M.Sc.. for carrying out the statistical analyses, and Ms. Ritva Vesanto and Ms. Hilkka Jarventaus for skillful technical assistance. The study has been financially supported by the Social Insurance Institution of Finland and Finska Lakaresallskapet.
REFERENCES Bingham, E., Pfitzer, E. A., Barkley, W., and Radford, E. P. (1968). Alveolar macrophages: Reduced number in rats after prolonged inhalation of lead sesquioxide. Science 162, 1297-1299. Bruch, J., Brockhaus, A., and Dehnen. W. (1974). Local effects of inhaled lead compounds on the lungs. International Symposium. Recent advances in the assessment ofthe health effects of environmental pollution. Paris, June 24-28, p. 35. Cogbill, E. C.. and Hobbs. M. E. (1957). Transfer of metallic constituents of cigarettes to the mainstream smoke. 7’ohocco 144, 24-29. Dahlman, T. (1966). Effect ofcigarette smoke on ciliary activity. Amer. Rrr. Rrspir. Dis. Soppl. 93, 108. Dames. R. H., Smith, D. W., Feliciano, A., and Trout, J. R. (1972). Air levels of lead inside and outside of homes. Ind. Med. Surg. 41, NO. 10, 2628. Hessel, D. W. (1968). A simple and rapid quantitative determination of lead in blood. At. Absorpt. Ncwd. 7, 55-56. Hofreuter, D. H., Carcott, D.V.M.. Keenan, M. S., and Xintaras. C. (1961). The public health significance of atmospheric lead. Arch. Environ. Health 3, 82-88. Ide, G., Suntzeff, V.. and Cowdry, E. V. (1959). A comparison of the histopathology of tracheal and bronchial epithelium of smokers and nonsmokers. Cancer (Brrrssels) 12, 473-484. Jones, R. D., Commins. B. T.. and Cemik. A. A. (1972). Blood lead and carboxyhaemoglobin levels in London taxi drivers. Lancer 2, NO. 7772. 302-303. Lehnert. G., Schaller, K. H.. Kuhner, A., and Szadkowski, D. (1967). Auswirkungen des Zigarettenrauchens auf den Blutbleispiegel. Int. Arch. Gewvrbrputhol. Gr+~~erhrhyg. 23, 358-363. McLaughlin, M., and Stopps. G. J. (1973). Smoking and lead. Arch. .En~?ron. Hecrlth 26, 131-136. Nordman, C. H. (1975). “Environmental Lead Exposure in Finland.” Academic dissertation. University of Helsinki.
SMOKING
AND
BLOOD
LEAD
355
Szadkowski, D.. Schultze. H., Schaller, K. H.,and Lehnert, G. (1969). Zurokologischen Bedeutungdes Schwermetallgehaltes von Zigaretten. Arch. Hq. 1.53, 1-8. Tepper. L. B., and Levin, L. S. (1972). “A Survey of Air and Population Lead Levels in Selected American Communities.” Department of Environmental Health. Kettering Laboratory. University of Cincinnati. Thomas, H. V., Milmore. B. K.. Heidbreder, G. A., and Kogan. B. A. (1967). Blood lead of persons living near freeways. Arch. Environ. Nrolth 15, 695-702. Tola. S. (1973). The effect of blood lead concentration. age, sex. and time of exposure upon erythrocyte fi-aminolevulinic acid dehydratase activity. Work Eni,irorr. Hrulth 10, 2635. Tola, S., Hernberg, S., and Vesanto, R. (1976). Occupational lead exposure in Finland. VI. Final report. S~~crnll. J. Work, Enr,iron. Hrcrlth 2, 115-127. U.S. Department of Health, Education and Welfare, Publice Health Service. Division of Air Pollution. (1975). “Survey of Lead in the Atmosphere ofThree Urban Communities.” Public Health Service Publication 999-AP-12. Cincinnati, Public Health Service. Warr. G. A.. Martin, R. R., and Gentry, L. 0. (1975). Alterations in pulmonary alveolar macrophages from young cigarette smokers. Irt “Proceedings of the XXIIIrd Conference of the International Union Against Tuberculosis, Mexico City. September 25.”
and Blood Lead Concentrations in Workers and an Unexposed Population S. TOLA
AND C. H. NORDMAN
Received
April
30. 1976
Blood lead (Pb-B) concentrations were measured and the smoking history was taken from 355 men representing the general population and 2209 men occupationally exposed to lead. No association between smoking and Pb-B could be demonstrated in the men from the general population, but a dose-response relationship was found between the amount of smoking and the Pb-B concentrations of men occupationally exposed to lead. Smokers had statistically significantly higher Pb-B levels than nonsmokers. This result can probably be attributed to the contamination of fingers and cigarettes in the lead-exposed workplaces rather than to the small amount of lead contained in the cigarettes. The deleterious effect of smoking upon the lung clearance mechanism can also be a contributing factor.
INTRODUCTION
Smoking has been claimed to be associated causally with the higher blood lead (Pb-B) levels found in smokers as compared to nonsmokers (Hofreuter et al., 1961; Tepper and Levin, 1972). On the other hand, some recent studies have failed to demonstrate a difference between the two groups (Daines et nl., 1972; Lehnert et ~1.. 1967; McLaughlin and Stopps, 1973; Nordman, 1975; Thomas rt cl/. , 1967). All these reports have dealt with people without any known occupational lead exposure. In a survey of the Pb-B levels among the general Finnish population (Nordman, 1975) and one of workers occupationally exposed to lead (Tola et ctl., 1976), information was also collected on smoking habits. In the present investigation we have used the data of both surveys to study the association between the smoking and the Pb-B concentrations of men with different degrees of occupational lead exposure. MATERIAL
Between 1970 and 1973 a survey on the lead exposure of the general population was made by one of us (Nordman, 1975). From this material all men (N = 355) with accurately recorded smoking histories and no occupational or related exposure to lead were selected for the present study. Their mean age was 37 (SD 13) years. At the time of the survey on the genera1 population, 2209 workers occupationally exposed to lead in 30 different types of work were also studied (Tola rt al., 1976). Accurate information with regard to smoking habits was available for 2108 men, whose mean age was 36 (SD 12) years. From both the genera1 population and lead exposed workers, only those who either smoked cigarettes, were nonsmokers, or had stopped smoking were included. Those reporting pipe or cigar smoking were excluded because the group was small and also too heterogeneous with regard to smoking habits.
METHODS
The Pb-B concentrations were measured by the atomic absorption spectrophotometric method described by Hessel(l968). The method error for determinations from duplicate samples was 2.1 &IO0 ml. The intra- and interlaboratory method control has been described earlier (Nordman, 1975; Tola, 1973). Smoking histories were collected with a self-administered questionnaire. The following smoking categories were used: (1) has never smoked, (2) has smoked previously but has stopped smoking, (3) smokes l-20 cigarettes daily, (4) smokes more than 20 cigarettes daily, (5) smokes a pipe or cigars. Category 5 was excluded from the analyses. Since a more common occurrence of heavy lead exposure among the heavier smokers could bias the results, the material was arbitrarily stratified into three lead exposed groups, i.e., heavy, moderate, and slight. Previous experience determined the stratification in terms of types of work. For example, workers in storage battery manufacturing and shipbreaking were considered as heavily exposed, those in foundries and ammunition factories were considered moderately exposed, and those working in service stations and electric bulb factories were considered slightly exposed. In addition to exposure stratification the workers were also grouped by age: ~34, 35-49, and 150 years. RESULTS
Table I shows the means and standard deviations of the blood lead concentrations of the men from the general population and Table 2 presents those from the lead exposed workers. There were no statistically significant differences between the different smoking categories in the general population, but the difference between occupationally exposed smokers and nonsmokers was statistically significant. Moreover, Pb-B values tended to increase concomitantly with more smoking. These differences were statistically significant also in the age groups of ~34 years and 3.5-46 years. In the eldest age group the Pb-B values of the smokers were higher (mean 26.9) than those of the nonsmokers (mean 23.8), but this difference was not statistically significant. The Pb-B concentrations of the different occupationally exposed strata are shown in Tables 3-5. In each stratum the Pb-B concentrations of smokers were
Blood Smoking
category
Cigarettes daily 321 I - ‘0 Stopped smoking Never smoked o Calculations
were
performed
!V
Mean
30 131 49 135
10.8 11.4 10.8 10.1
after
logarithmic
lead concentration
transformation.
Mean
+ SD
14.8 16.2 15.9 14.4
(&I00
ml) Mean
- SD
7.9 x.1 7.3 7.2
252
TOLA
AND
NORDMAN
Blood Smoking
category
Cigarettes daily 321 1 - 20 Stopped smoking Never smoked (i Calculations
were
performed
N
Mean
296 947 355 537
30.1 28.5 25.9 24.4
after logarithmic
lead concentration Mean
(&IO0
+ SD
ml) Mean
51.3 48.1 42.5 40.3
transformation.
~ SD
17.6 16.8 15.8 14.8
F = 13.40. & = 3; 2104. P < 0.001.
statistically significantly higher than those of nonsmokers, and also the trend of higher Pb-B values with more smoking was evident. Both this trend and the statistically significant differences between smokers and nonsmokers could be demonstrated also in the age groups of s34 years and 3549 years. In the eldest age group statistical significance was not achieved although the trend of increasing Pb-B values with increasing smoking within different exposure strata was observed also for this age group. DISCUSSION
In our study the Pb-B levels of the general population revealed no differences between smokers and nonsmokers. This result coincides with the results of several recent studies (Daines et crl., 1972; Jones ef al., 1972; Lehnert et al., 1967; McLaughlin and Stopps, 1973; Nordman, 1975; Thomas et al., 1967). Other investigators have, however, claimed that smokers do have higher Pb-B levels than nonsmokers (Hofreuterrt al., 1961; Tepperand Levin, 1972; U.S. Dept. of Health, Education and Welfare, 1975). The elevated Pb-B levels of smokers without occupational lead exposure have been attributed to the small amounts of lead in tobacco leaves because of the former use of leaded pesticides (Cogbill and Hopps, 1957). Szadkowski and his colleagues (1969) determined that 3.1 pugis the average daily amount of lead absorbed from cigarette smoke for an average smoker (17 TABLE BLOOD
LEAD EXPOSED
CONCENTRA TO Lt.4~
3
I 10~s (/&lo0 ml) OF WORKERS HEAVILY AFFORDING ‘I’O SMOKING C.~ITSXIR~”
Blood Smoking
category
Cigarettes daily 321 1 - 20 Stopped smoking Never smoked 0 Calculations
were
performed
N
Mean
50 198 54 74
55.8 47.7 43.8 38.4
after
logarithmic
lead concentration Mean
+ SD
(&IO0
ml) Mean
88.5 78.6 78.1 65.5 transformation.
F = 5.93.
- SD
35.2 28.9 24.6 22.5 & = 3;372.
P < 0.001.
253
Blood Smoking
category
Cigarettes daily 321 I ~ 70 Stopped smoking Never smoked ” Calculations
were
performed
N
Mean
I74 419 701 313
29.1 26.3 ‘5.1 24.6
after logarithmic
lead concentration Mean
+ SD
(pg/lOO
ml) Mean
43.9 40.0 37. I 37.9
transformation.
- SD
19.3 17.3 17.0 15.9
F = 28.33. c(t‘ = 3;1 114. P < 0.001.
cigarettes/day). This amount is small in comparison with that absorbed daily from food, even though that absorbed from food displays a large individual and day-today variance (Nordman, 1975), and in comparison with the amount absorbed from air. Therefore, it seems questionable whether such a small amount would be reflected in the Pb-B level. Nevertheless, the contribution of lead from smoking to the daily lead absorption of the genera1 population can scarcely be regarded as hazardous to man’s health. Smoking in lead-exposed work environments seems to cause elevated Pb-B levels in smokers as compared to nonsmokers. Moreover, our results indicate a dose-response relationship between smoking and Pb-B concentrations. Although such a relationship was not statistically significant in the oldest age group of our study, a difference did exist between the Pb-B levels of smokers and nonsmokers. Thus the results within this group were considered consistent with the hypothesis of a causal association. The lead exposure provided by smoking among lead-exposed workers is different from that of the general population. The contamination of cigarettes and fingers with lead particles probably affects exposure more than the lead content of the cigarette itself. This effect seems to be more pronounced in the most exposed occupations; however, the wider range of the Pb-B values determined in this group contributed to the greater differences found within the group. Part of the effect of smoking on lead absorption in workers exposed to lead may
Smoking
category
Cigarettes daily 230 1 ~ 20 Stopped smoking Never smoked a Calculations
were
performed
N
Mean
95 170 99 150
2.7 31.5 20.7 19.3
after
logarithmic
transformation,
Mean
+ SD
Mean
14.6 14.2 13.5 12.2
35.2 35.6 31.8 30.8 F = 4.46. #
- SD
= 3:6)0.
p < 0.01.
254
TOLA
AND
NORDMAN
be explained by an impairment of the lung defense mechanisms, The inhalation of cigarette smoke is known to depress ciliary activity and the transportation of mucus in a variety of mammalian species (Dahlman, 1966). There is also evidence indicating that the length of cilia is decreased and the percentage of ciliated cells is diminished in human smokers (Ide et al., 1959). Moreover, Warr et a/. (1975) have recently reported that the alveolar macrophages of young smokers display a decreased phagocytic capacity. In addition lead has repeatedly been shown to decrease the number of alveolar macrophages in animals distinctly and thereby impair lung clearance (Bingham et al., 1968; Bruch et al., 1974). Theoretically, the combined effect of smoking and lead exposure on alveolar macrophages should be more severe than that of lead exposure alone. The importance of this combined effect remains to be assessed. Nevertheless, the effect of smoking on lung defense mechanisms is deleterious and is likely to cause an increase in the retention of such inhaled substances as lead particles in inhaled air and cigarette smoke. Our findings indicate a dose-response relationship between the smoking of occupationally exposed workers and elevated Pb-B levels. Because one possible source of the exposure is the environmental contamination offingers and cigarettes, personal hygiene ought to be emphasized and smoking in workrooms must be prohibited. Of course the ultimate solution would be for workers to stop smoking completely. ACKNOWLEDGMENTS We wish to thank Raili Vilhunen, M.Sc. (eng.), for the supervision of the laboratory analyses, Sisko Asp, M.Sc.. for carrying out the statistical analyses, and Ms. Ritva Vesanto and Ms. Hilkka Jarventaus for skillful technical assistance. The study has been financially supported by the Social Insurance Institution of Finland and Finska Lakaresallskapet.
REFERENCES Bingham, E., Pfitzer, E. A., Barkley, W., and Radford, E. P. (1968). Alveolar macrophages: Reduced number in rats after prolonged inhalation of lead sesquioxide. Science 162, 1297-1299. Bruch, J., Brockhaus, A., and Dehnen. W. (1974). Local effects of inhaled lead compounds on the lungs. International Symposium. Recent advances in the assessment ofthe health effects of environmental pollution. Paris, June 24-28, p. 35. Cogbill, E. C.. and Hobbs. M. E. (1957). Transfer of metallic constituents of cigarettes to the mainstream smoke. 7’ohocco 144, 24-29. Dahlman, T. (1966). Effect ofcigarette smoke on ciliary activity. Amer. Rrr. Rrspir. Dis. Soppl. 93, 108. Dames. R. H., Smith, D. W., Feliciano, A., and Trout, J. R. (1972). Air levels of lead inside and outside of homes. Ind. Med. Surg. 41, NO. 10, 2628. Hessel, D. W. (1968). A simple and rapid quantitative determination of lead in blood. At. Absorpt. Ncwd. 7, 55-56. Hofreuter, D. H., Carcott, D.V.M.. Keenan, M. S., and Xintaras. C. (1961). The public health significance of atmospheric lead. Arch. Environ. Health 3, 82-88. Ide, G., Suntzeff, V.. and Cowdry, E. V. (1959). A comparison of the histopathology of tracheal and bronchial epithelium of smokers and nonsmokers. Cancer (Brrrssels) 12, 473-484. Jones, R. D., Commins. B. T.. and Cemik. A. A. (1972). Blood lead and carboxyhaemoglobin levels in London taxi drivers. Lancer 2, NO. 7772. 302-303. Lehnert. G., Schaller, K. H.. Kuhner, A., and Szadkowski, D. (1967). Auswirkungen des Zigarettenrauchens auf den Blutbleispiegel. Int. Arch. Gewvrbrputhol. Gr+~~erhrhyg. 23, 358-363. McLaughlin, M., and Stopps. G. J. (1973). Smoking and lead. Arch. .En~?ron. Hecrlth 26, 131-136. Nordman, C. H. (1975). “Environmental Lead Exposure in Finland.” Academic dissertation. University of Helsinki.
SMOKING
AND
BLOOD
LEAD
355
Szadkowski, D.. Schultze. H., Schaller, K. H.,and Lehnert, G. (1969). Zurokologischen Bedeutungdes Schwermetallgehaltes von Zigaretten. Arch. Hq. 1.53, 1-8. Tepper. L. B., and Levin, L. S. (1972). “A Survey of Air and Population Lead Levels in Selected American Communities.” Department of Environmental Health. Kettering Laboratory. University of Cincinnati. Thomas, H. V., Milmore. B. K.. Heidbreder, G. A., and Kogan. B. A. (1967). Blood lead of persons living near freeways. Arch. Environ. Nrolth 15, 695-702. Tola. S. (1973). The effect of blood lead concentration. age, sex. and time of exposure upon erythrocyte fi-aminolevulinic acid dehydratase activity. Work Eni,irorr. Hrulth 10, 2635. Tola, S., Hernberg, S., and Vesanto, R. (1976). Occupational lead exposure in Finland. VI. Final report. S~~crnll. J. Work, Enr,iron. Hrcrlth 2, 115-127. U.S. Department of Health, Education and Welfare, Publice Health Service. Division of Air Pollution. (1975). “Survey of Lead in the Atmosphere ofThree Urban Communities.” Public Health Service Publication 999-AP-12. Cincinnati, Public Health Service. Warr. G. A.. Martin, R. R., and Gentry, L. 0. (1975). Alterations in pulmonary alveolar macrophages from young cigarette smokers. Irt “Proceedings of the XXIIIrd Conference of the International Union Against Tuberculosis, Mexico City. September 25.”
