P.1 

OAR Box 1131 

Prepped by Ollie Stewart 

Document Number: 

54) 11-1-71 

Docket Number: 

A-83-22 

Printed 4/21/2008 2:34:09 PM Sheet 54 of 162 
P.2 

--•-•--*••*• f r^B j 

AERE - R 9198 

:"S*;. iv ^ 

INVESTIGATIONS INTO LEAD FROM MOTOR VEHICLES 

A.C. Chattberlain 

M.J. Heard 

P. Little 

D. Newton 

A.C. Wells 

R.D. Wiffen 

Report of work at AERE, Harwell sponsored by the member 

companies of the Institute of Petroleum, Department of Energy, 

Departinent of the Environment, Department of Health and Social 

Security and International Lead Zinc Research Organisation. 

Environmental & Medical Sciences Division, 

AERE, HARWELL 

November 1S78 

HL78/4122 (C.10) 

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• • • 

t. 

2. 

3. 

-

4. 

5. 

CONTENTS 

Sunmary 

Introduction 

2.1 

2.2 

2.3 

2.4 

2.5 

Envi 

3.1 

3.2 

3.3 

3.4 

3.5 

3.6 

3.7 

Origins and objects of the work 

Previous publications 

• 

Reasons for environmental measurements 

203 

Reasons for Pb inhalation and injection experiments 

Reasons for ingestion experiments 

ronmental measurements 

Emission of exhaust lead from vehicles 

Deposition of lead near roads 

Comparison of rates of emission and deposition of lead 

The possible use of shelter belts for Limiting dispersal of lead 

Concentrations of lead in air 

(a) Roadside measurements 

(b) Measurements in cars 

(c) Variation of airborne lead with distance 

(d) Urban and suburban sites not adjacent to 

(e) Enclosed car park 

Particle size analyses 

(a) Objectives and methods 

(b) Motorway aerosols 

(c) Urban, suburban and rural areas 

(d) Enclosed car park 

Chemical composition of exhaust lead 

Inhalation of stable lead 

4.1 

4.2 

4.3 

Methods of measurement 

Inhalation experiments in the field 

Comparison of field and laboratory methods 

Inhalation of radioactive lead aerosols 

5.1 

5.2 

5.3 

Object of experiments 

Preparation and inhalation of labelled aeroso] 

(a) Wind-tunnel aerosols 

(b) Box aerosols 

Deposition of labelled aerosols in the lung 

5.3.1 Wind-tunnel aerosols 

5.3.2 Box aerosols 

5.3.3 Comparison with other published work 

5.3.4 Variation between individuals 

ISBN 0-70-580650-2 

-2-

from 

main 

s 

road 

roads 

".i. '-">"»FT»r » 1 ' » ' trai'T 

Page No. 

9 

12 

12 

12 

13 

14 

14 

15 

15 

15 

16 

17 

17 

ie 

19 

19 

20 

21 

21 

21 

22 

23 

25 

25 

41 

41 

42 

43 

50 

50 

V; 

51 

52 

52 

52 

53 

54 

54 

I 1 T 

\ 

*-~« 

\ 

t 

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P.4 

CONTENTS ICont'd) 

« 

6. Clearance of labelled aerosols from the lung 

6.1 Object of experiments 

6.2 Methods of measuring rate of clearance 

6.3 Results of lung clearance experiments 

6.4 Transfer from lung to blood 

6.5 Dosage of stable lead 

7. Injection experiments 

7.1 Object of experiments 

7.2 

8. 

10. 

r.3 

Methods 

203 

Pb in blood following injection 

7.3.1 Interchange with extra-cellular fluid 

203 

7.3.2 Levels of Pb in plasma 

7.3.3 Transfer from blood to sites of storage 

203„ 7.3.4 Pb in blood from one dav onwards 

203 Excretion of Pb 

8.1 Object of measurements 

6.2 Methods 

8.3 Excretion in urine 

8.4 Endogenous fecal excretion 

8.5 Total excretion 

8.6 Excretion in relation to 

8.7 Relation of urinary excretion to 

203Pb 

203 Pb in blood 

203, 

Pb in plasma 

Ingestion experiments with 

9.1 Object of experiments 

9.2 Methods 

9.3 Uptake from the gut 

203 

9.4 Observations on absorbed Pb following ingestion 

9.4.1

 203Pb in blood 

9.4.2 Appearance of systemic lead following ingestion 

9.4.3 Excretion 

9.5 Summary of results of ingestion experiments 

Synthesis of AERE and other results 

10.1 Introduction 

10.2 Uptake and storage of lead in Kehoe's experiments 

10.3 Uptake and storage of lead in UCLA experiments 

10.4 Elevation of blood lead in experimental exposure of subjects 

to PbA 

(a) Kehoe's subjects 

(b) Griffin et aL's subjects 

(c) Tola's subjects 

Pag.- Nc. 

65 

65 

65 

65 

66 

67 

82 

82 

82 

82 

62 

83 

63 

84 

90 

90 

90 

91 

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93 

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112 

114 

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120 

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CONTENTS (Cont'd) 

10.5 Surveys of blood lead versus air lead in various regions 

10.6 Blood lead versus water lead 

10.7 Lead in children's blood 

10.8 Resorption of lead from bone 

(a) Kehoe's experiments 

(b) Bone lead versus age 

(c) Blood lead versus age 

(d) Blood lead in occupational versus non-occupational 

groups 

(e) Isotopic ratios in lead and blood 

204 

(f) UCLA experiments with Pb 

10.9 Possible scheme of uptake and excretion of lead 

10.10 Conclusions 

Acknowledgements 

References 

Table 3.1 

Table 3.2 

Table 3.3 

Table 3.4 

Table 3.5 

Table 3.6 

Table 3.7 

Table 4.1 

Table 4.2 

Table 4.3 

Table 5.1 

Table 5.2 

TABLES 

Lead deposition rates at various locations 

Measurements of lead-in-air beside motorways and other 

streets 

Measurements of airborne lead in carborne surveys 

Measurements of airborne lead at fixed site s 

Particle size analyses 

Categories of particles in electron micrographs 

Volumetric-mean particle diameters 

Deposition in lung of environmental lead 

Deposition in lung of stable aggregated exhaust Pb using 

field equipment 

Percentage deposition by radioactive and stable lead 

analysis 

203 Particle size of wind-tunnel ' Pl> v.xtaunt aerosol* 

Aggregated aerosols - Andersen Impactor data 

I) 

2) 

203, 

i 

203, 

i 

203„ 

Pb-labelled exhaust aerosols (1976-1977) 

Pb-labelled lead compounds (1976-1977) 

Table 5.3 

Table 5.4 

3) '""Pb-labelled exhaust aerosols (1975) (Wells et al. 1977) 

Deposition in lung of wind-tunnel aerosols 

Deposition in lung of aggregated exhaust and other 

labelled aerosols 

203 PbPage No. 

120 

121 

123 

123 

123 

124 

124 

124 

124 

125 

125 

127 

14C 

14G 

.27 

28 

29 

29 

30 

31 

31 

45 

46 

AT, 

SC> 

Table 5.5 Variation of respiratory deposition between two subjects 

57 

58 

56 
P.6 

"TT'-ITTTrTf"--'-" 

CONTENTS (Cont'd) 

•>03 Table 6.1 Lung clearance following inhalation of ' Pb-labelled 

aerosols. Comparison of exponential components or the 

observed mean clearance curves for six different aerosol* 

203 Table 7.1 Possible distribution of Pb after intravenous saline 

injection 

203 Table 7.2 Mean percentage of absorbed Pb appearing in blood at the 

peak for various groups of experiments 

203 Table 7.3 Peak levels of Pb in blood following intravenous injection. 

Comparison of subjects with more than one attninistrati on 

Table 7.4 Biological half-lives of Pb in blood following intravenous 

saline injection compared with other modes of intake 

(individual values for saline injection experiments) 

Table 6.1 Excretion of Pb following intravenous saline injection -

1977 series 

Table 8.2 Comparison of endogenous fecal and urinary excretion in 

different series of experiments 

*Wi**> 

Table 8.3 Accounting for Pb in saline injections (1977 series) 

203 Table 8.4 Urinary and fecal excretion of Pb relative to concentrations 

in *hole blood following injection 

203 Table 8.5 Comparison of the observed biological half-lif e of Pb in 

Pagr No. 

68 

Table 8.6 

Table 9.1 

Table 9.2 

Table 9.3 

Table 9.4 

Table 9.5 

Table 10.1 

Table 10.2 

Table 10.3 

Table 10.4 

Table 10.5 

Table 10.6 

Table 10.7 

Table 10.8 

blood with the calculation (F + U) half-lif e from Table 8.4 

203 Relation between Pb in urine and plasma, 0-46 hours 

203 Percentage uptake of Pb from the gut 

Percentage uptake of lead from the gut: comparison of 

published data 

203 The hierarchy of subjects in Pb injection experiments 

203 Percentage uptake in gut of Pb-labelled exhaust aerosols 

3 0 *"r 

Half-life in blood of Pb following ingestion compared 

with values following saline injection 

Storage of lead by Kehoe's subjects receiving daily oral 

doses 

Uptake, excretion and storage of lead in Kehoe'• subjects 

MR and EB 

Lead balance in Kelioe's subject PC before, during and after 

exposure to airborne lead in an experimental chamber 

204 Endogenous fecal excretion of Pb by UCLA subjects 

204 Uptake and storage of Pb in UCLA subjects given daily 

oral doses 

204 

Estimates of half-life of Pb in blood of UCLA subjects 

204 

Pb and total Pb in diet and blood of UCLA subjects 

Respired lead intake by three methods (Mg/d) 

85 

86 

66 

94 

94 

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105 

105 

106 

107 

107 

129 

129 

130 

130 

131 

131 

132 

132 

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•wpTT' T '"""flf ""•""•"*'" 

Table 

Table 

Table 

Table 

Table 

Table 

Table 

Table 

Table 

Table 

10.9 

10.10 

10.11 

10.12 

10.13 

10.14 

10.15 

10.16 

10.17 

10.16 

Table 10.19 

Table 10.20 

Table 10.21 

CONTENTS ( Cont'd) 

Sunmary of results of experimental exposure to lead in air 

Fit of exponential curves to PbB of Dannemora subjects in 

Fig. 10.3 

Mean blood lead in populations in California 

Predicted mean childhood blood lead (pg/iOO ml) for 

various air and soil lead concentrations near smelter 

Elevation of blood lead from oral intake of lead 

Blood lead and dietary lead 

Ratio of intakes of air and food per unit blood volume for 

10 year old children and adults 

Lead in blood of children and mothers 

Lead in tissues at post mortem (Barry 1975) 

Scheme of uptake and excretion of lead by adult male in 

urban district of UK 

Relative contributions to uptake of lead in analysis of 

Ainsworth et al. (1977) 

Summary of estimates of elevation of blood lead of adults 

from exposure to air lead 

Summary of estimates of ratio of contributions of air lead 

to other lead intakes (adults) 

Page No. 

133 

134 

134 

135 

133 

136 

136 

137 

137 

138 

138 

139 

139 

ILLUSTRATIONS 

Fig. 3.1 M4 motorway at Heston 

Fig. 3.2 Concentrations of Pb in air and rates of Pb deposition 

to grass across the M4 motorway 

Fig. 3.3 M40 motorway 

Fig. 3.4 Hogarth roundabout 

Fig. 3.5 Variation of concentration with distance from motorway 

Fig. 3.6 A typical motorway exhaust aerosol viewed by electron 

microscopy at three magnifications 

Fig. 3.7 Vehicle aerosols: size distribution of three classes of 

particle 

Fig. 3.8 Total particle size distributions at M4 (Heston and Hogarth 

roundabout) 

Fig. 3.9 Levels of airborne Pb in a small town 

Fig. 4.1 Subjects inhaling exhaust aerosol on the hardshoulder of 

the M4 

Fig. 4.2 Carborne inhalation equipment 

Fig. 4.3 Deposition of lead in lung in field experiments versus 

length of respiratory cycle 

32 

33 

34 

33 

36 

38 

39 

40 

47 

46 

49 
>TWYT~' ' -«T^»' ,

" - -TfrS P.8 

Fig. 5.1 

Fig. 5.2 

Fig. 5.3 

Fig. 5.4 

Fig. 5.5 

Fig. 5.6 

Fig. 6.1 

Fig. 6.2 

Fig. 6.3a 

Fig. 6.3b 

Fig. 6.4 

Fig. 0.3 

Fig. 6.G 

Fig. 6.7 

Fig. 6.6 

Fig. 6.9 

Fig. 6.10 

Fig. 6.11 

Fig. 6.12 

Fig. 7.1 

Fig. 7.2 

Fig. 7.3 

Fig. 8.1 

CONTENTS (Cont'd) 

Subject inhaling aerosol from wind-tunnel 

Wind-tunnel exhaust aerosols as used in inhalation 

experiments 

Deposition in lung of wind-tunnel aerosols 

203 _. , 

Deposition in lung of Pb-labelled aggregated aerosols 

1976-1977. Percentage deposition versus breathing cycle 

Deposition in lung of aggregated aerosols. Comparison of 

mean deposition curves 

A comparison of published data on deposition in lung of 

submicron particle s 

203„ 

Percentage of deposited " Pb remaining in lung, 

tunnel exhaust aerosols (0.02 Mm) 

203p 

7/7/ 

20 3„ 

Percentage of deposited Pb remaining in lung, 

exposed exhaust aerosol 7/7/76 

WinduA 

Percentage of deposited ""' Pb remaining in lung, Clean 

and carbonaceous exhaust aerosols 

203 

Percentage of Pb remaining in lung. Carbonaceous 

exhaust aerosols at times beyond 10 hours 

Percentage of deposited 

nitrate aerosols 

Percentage of deposited 

oxide aerosol? 

203, Pb remaining in lung. Lead 

203 Pb remaining in lung 

203, 

Lead 

Comparison of the lung clearance of various 

aerosols 

Pb-labelled 

Clearance of various exhaust aerosols from the lung 

Comparison of in vitro solubilities with lung clearance 

203 

Levels of Pb in blood following inhalation of exhaust, 

oxide or nitrate aerosols, or injection of PbCl, 

Lung clearance at different levels of stable lead deposition 

Relationship between stable lead dosage and peak levels in 

blood for individual subjects 

Normalised relationship between stable lead dosage and peak 

levels in blood 

203 

Levels of Pb in blood following intravenous injections 

of

 203 PbCl2 in saline 

203, 

Percentage of Pb in blood in the plasma 

203 

Pb in blood normali=ed to 100 at 60 h after intravenous 

saline injection of

 203 PbCl, 

of IT 

Rates of trx'.rrrtion of ' Pb in urine during the first 

34 hours following intakr 

Pagr- No. 

5<* 

60 

61 

62 

63 

64 

69 

70 

71 

72 

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75 

76 

i I 

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89 

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P.9 

Fig. 8.2 

Fig. 8.3 

Fig. 8.4 

Fig. 9.1 

Fig. 9.2 

Fig. 9.3 

Fig. 10.1 

Fig. 10.2 

Fig. 10.3 

Fig. 10.4 

Fig. 10.5 

Fig. 10.6 

CONTENTS (Cont'd) 

30"*L 

Rate of excretion of Pb in urine during the first 

36 hours after inhalation. Comparison of: 

(i) 5 different aerosols for one subject 

(ii) 4 different subjects for one aerosol 

203 Excretion of Pb in urine and feces following: 

(a) inhalation of motor exhaust aerosols, and 

(b) I.V. injection of

 203PbCl2 

203 Excretion of Pb in urine expressed in terms of blood 

plasma 2°3Pb. Comparison of intravenous saline injection 

and inhalation 

203 

Percentage uptake from the gut of PbCl_ taken with and 

without accompanying food 

203 Variations of level of Pb in whole blood for various 

modes of intake 

203 Pb in legs following ingestion and inhalation 

204 

Pb in bldod of UCLA subjects (Rabinowitz et al. 1976b). 

Curves are fitted by method (c) of Section 10.3 

204 

Loss of Pb from blood of four subjects after withdrawal 

of isotope from diet (Rabinowitz et al. 1976b) 

Blood lead of Dannemora subjects exposed to mean 24-hour 

air concentrations of 10.4 pg/m3 (above) or 3.1 Pg/m3 

(below) 

Increase of PbB in Tola et aL's subjects on beginning work 

in lead industry 

PbA and PbB in Tokyo 

Lead in skeleton at death, normalised to 70 kg body weight 

(Barry 1975) 

Page No.. 

98 

99 

100 

ioe 

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110 

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P.10 

I. Sui'nmarv 

I 

Thi's report gives th-; results of three years' work on lead aerosols in the environment 

and the laboratory. The >i; :ake of both radioactive and stable lead by human volunteers has 

been measured, with the object of estimating the uptake by humans of lead from petrol driven 

vehicles, and also the contribution of this to the total uptake of lead. Radioactive tracers 

were used to detenr.ine the effect of chemical composition of lead aerosols on uptake, and 

also to compere uptake frun lun& and gut. The effects of lead on health were not included 

in the work. 

Earlier work carried out in this project has been published and is reviewed. Exhaust 

203 

aerosol labelled with Pb was inhaled by volunteers and the deposition in the lung and 

uptake by blood measured by means of the radioactive tracer. The results were used to 

calculate a vaiue for the relation between blood lead and air lead expressed as 

_ Elevation of blood lead (ug/100 ml) , 

a ~ Average 24-hour exposure to air lead (pg/m ) 

A calculation based on 35% deposition of the inhaled aerosol in the lung, 509E transfer of 

the lead to red cells and a 16-day biological half-life in blood, gave a value ofa of about 

unitv. The work indicated the significance of particle size on deposition in the lung. 

Ambient measurements 

The particle size, concentration and dispersion of ambient lead aerosols were assessed 

at a variety of roadside sites to determine the typical nature of airborne lead. The 

results indicate that lead emitted from cruising vehicles, as on a motorway, is mainly as 

very small discrete particles of about 0.03 pm diameter. Under urban driving conditions, 

wit! vehicles accelerating strongly, and when the aerosol had'aged' as in car parks or in 

the eountrxside. a wider spectrum of particle size was found, wit! some lead attached to 

agglomerate particles of 0.2-2 (in diameter. Contrary to reports from the USA, very little 

lead was associated -.vith particles greater than 5 pm. 

Correlation of measurements by various authors shows that roadside concentrations are 

usually about 2 ug/m for each 1000 petrol-driver vehicles per hour, but are higher on 

gradients and in poorly ventilated situations. 

Lead concentrations decline rapidly with distance frcm a road. The main factor is i, 

upward dispersion of the plume rather than deposition of the lead; only about 10£ of the R| 

airborne lead seeiis to be deposited within 100 m. \ ' 

Dispersion calculations relating traffic flow to the concentration of airborne lead at 

various distances from a road suggest that, averaged over 24 hours, for 1000 Vh there is a 

zone about 15 m wide on either side of the road in which the concentration exceeds I ..g/m . 

For a very busy motorway carrying 4000 Vh~ the equivalent zone is 100 m wide. Concentrations in urban houses are about 6<JZ of those outside. 

Inhalation measurements 

Volunteers inhaled fresh and aged lead aerosol labelled with the radioactive isotope 

203 

Pb. When fresh aerosol was diluted directly from motor exhaust in a wind tunnel the 

stable lead concentration was about 40pg/m . For a respiratory cycle of 15 breaths/min. 

there was 4Q"" deposition in the lung with a mean particle size of 0.04 pm and 70S deposition 

" 9 -
P.11 

with 0.02 um particles. Deposition was estimated from the concentration in the inhaled and 

203 exhaled air, and also from external gamma-ray counu: of the Pb in the Aung. 

Alternatively, when the exhaust was allowed to aggregate in a box for an hour or two 

before inhalation, giving higher lead concentrations snd a particle size about 0.5 pm, three 

separate series of experiments gave 175?, 20*? and 23*? for 15 breaths/min and 1 litre tidal 

volume. Not unexpectedly, deposition always increased with a slower breathing cycle, though 

the increase differed between the three series. 

When volunteers inhaled the ambient lead aerosol while seated near a motorway or travelling in cars in heavy traffic, the average deposition (deduced from the lead concentrations 

in the inhaled and exhaled air) was 6l£ near the motorway, 64?t near a busy roundabout, and 

48r- alon«g urban roads. The results near the motorway were in line with those for the wind-

^ — - — . —— ~ . ___._———— — — • 

tunnel experiments. Those from the urban roads were higher than expected from the laboratory 

work for reasons that were not fully understood. Impaction of larger particles in the urban 

aerosol in the Upper respiratory tract may have contributed to its higher deposition. 

Removal from the lung 

203 One object of the inhalation experiments with Pb was to examine whether the particle 

size, chemical composition or total mass of the lead-bearing aerosol affected the rate of 

removal of lead from the lung to the blood stream. Only small differences were found when 

fresh, aged and carbonaceous exhaust aerosol were compared. Also, aerosols of lead oxide 

and lead nitrate were removed from the lung at a similar rate to exhaust aerosol. The uptake 

was rapid at first, then slower, but in all experiments (except one 1973 experiment with L'.V. 

irradiated aerosol) over 8G"*c of the lung burden had gone by 24 hours after inhalation. The 

fraction of the initial lung budren present in blood 30 hours after inhalation was remarkably 

constant. It is believed that most of the lead not attached to red cells at this time was 

elsewhere in soft tissues, or in bone. Not more than a small percentage of the initial lead 

deposited in the lung had been removed by mucociliary action and swallowed. Differences in 

aqueous solubility as between lead oxide and nitrate, fresh and carbonaceous pyhanpt apmania 

and exhaust aerosols exposed to sunlight may have made some difference to the rate of clgar_-

ance from the lung, but not enough to affect significantly the relation between air lead and 

blood lead 

Removal from blood, and excretion 

203 Sequential samples of venous blood were taken up to 14 days afte r injection of Pb. 

Radioactive decay made it impossible to extend the measurements further. Over the period of 

203 

measurement, the Pb disappeared from blood exponentially with a biological half-lif e of 

16.3 _* 1.1 days (mean and standard error). After inhalation experiments, the half-lif e was 

16.4 ^ 0.7 days. The 18-day half-lif e agrees betttr with the results of UCLA workers using 

"" 204 

the stable isotope Pb. 

203 Urinary and fecal excretion of Pb was measured for 14 days afte r intravenous 

203 injection of PbCl, in saline solution. This excretion, averaging 0.83%of the dose per 

50*5. day in urine and 0.41% per day in feces, accounted for the reduction in the Pb in the 

subject's body as measured by external ^amma ray counting. This showed that other routes 

of excretion (for example in sweat) were unimportant. The rati o FA ' of endogenous fecal 

to urinary excretion was 0.5. Knowledge of this rati o assists the interpretation of 

10 -
experi.»ent=. such as those of ke: ~ \ in winch subjects arc given oral dose* of lead. Endogenous recal lead is then masked reabsorbed oral lead, but if Uie F^A1 ratio ran he 

estimated, the uptake from the £ of an oral dose can be estimated from the uriiiurv 

excretion. 

203 The uptake of Pb from the jut after oral doses was also measured. Thc average 

uptake of soluble PbO, was 45% when the subject had fasted overnight, but only Tl when hetook the dose with a meal. With relatively insoluble PbS, the average uptakes were 12^ and 

6r"i. There was considerable subject to subject variation, which, if it applied to uptake of 

stable lead in rood and drink would be enough in itself to explain the variation of blood 

lead in normal subjects. 

Relation between blood lead and air lead 

The previous work suggested a value of unit\ for a, the relation between blood lead and 

air lead. Although the differences in results between the present work and the previews are 

not great, they indicate a revision Tor the value of a. The environmental lead inhalation 

experiments suggest that 502 deposition should be assumed for the average urban dweller, and 

651 for the small number of people continuously exposed to motorway exhaust lead. Also the 

percentage transfer from lung to blood should be increased slightly to 55%. A biological 

half-life of 18 days instead of 16 is indicated by the results of the injection experiments. 

204 

and this agrees better with work at UCLA using Pb. The net effect of these alterations 

is to double a from 1 to 2 pg/100 ml per pg/m . A further small increase might be needed to 

allow for long-term resorption of lead from bone, which cannot be demonstrated in the time203 scale of the Pb experiments. 

Other literature relevant to the estimation of a is reviewed at some length. The experiments of kehoe, in which subjects inhaled lead aerosols at concentrations ranging from 10 to 

5 

150 ug/m for a number of hours per day for many months, yield an average value of a --• 1.2ug/100 g 

per ug/m . There is some evidence that a decreases with increasing lead-in-air concentrations, 

probably on account of more rapid excretion of lead from the blood. The more recent exposure of 

volunteer subjects to lead in air (10.4 and 3.1 Pg/m0) at Dannemora, N.Y., gave a. = 1.5 and 1.7. 

Some recent epidemiological surveys relating blood lead with air lead are also reviewed. 

Contribution of airborne lead to total uptake 

The final section of the report reviews this and other work to evaluate the relative 

contribution of lead in air to the total uptake. 

The difficulty is to estimate the uptake of dietary lead from the gut. If Kehoe's lead 

balance experiments are re-analysed with tlie assumption that the ratio F A' of endoienou; 

203

 e 

fecal to urinary lead was 0.5 (as found in the Harwell Pb experiments), the fractional 

uptake from gut is found to average 0.15. A possible scheme of uptake and excretion can 

then be constructed, in which the uptake of lead from the lung in a person exposed to 

I Pg/m day in air is 7.5 pg/day, compared with 41 pg/day uptake from the gut. 

This approach indicates that the contribution of air lead to total uptake at this 

level of exposure is about 16%. At the highest levels to which people are continuously 

exposed (for example in houses adjacent to the busiest stretch of the M4), the contribution 

of air lead to total uptake would appear to be comparable with that from diet. However. 

for the majority of urban and rural residents, for whom airborne lead averages less than 

- 5 

o.a Pg/m , this work indicates that the contribution of air lead to total uptake is less 

than 10"*". 

- II -
P.13 

2. Introduction 

2.1 Ori. s and objects of the work 

The project started in 1974 with the objectives of determining the deposition in 

the human lung of lead from motor exhaust, the uptake to blood, and, as far as 

possible, the subsequent fate of the absorbed lead. A report on the first stage of 

the work was submitted in 1975 (subsequently substantially published). In 1976 a 

continuation of the project was undertaken with the objectives 

(a) to study the effects of chemical change, particle size and different modes of 

engine operation on the retention and rate of uptake in the lung of exhaust 

lead aerosols, at concentrations which are realistic in relation to ambient 

levels, 

(b) to establish more firmly the ratio between the amount of absorbed lead which is 

eventually excreted with the feces and that excreted with the urine, 

(c) to define the relative contributions of inhaled and ingested lead to overall 

lead absorption, 

(d) to attempt to determine the distribution and final location of absorbed lead not 

accounted for in the blood or by excretion, 

(e) to evaluate other published studies on the uptake, distribution within the body, 

retention and excretion of lead and to relate their findings to the present 

study. 

203 The original conception was to use a radioactive tracer ( Pb) to label the lead 

in petrol and thus enable the deposition in the lung and subsequent fate of the exhaust 

lead to be followed. The labelling allows the lead inhaled during a specific, short 

term experiment to be distinguished from the lead in the body originating from other 

sources. It was found that the particle size of the lead, which depends on the 

conditions of generation and storage of the aerosol, markedly affects the deposition 

in the lung, as would be expected from other work on inhalation of particles. It 

became evident that the published information on particle sizes of lead in the 

environment was inadequate, and a sampling programe was begun to obtain more information, with particular reference to possible differences in particle size under 

different environmental conditions. The concentrations of lead in air, near the M4 

motorway and near other heavily used urban roads were found to be high enough to 

enable the deposition in the lung of the ambient lead aeroco) to be nvaaurM hy «•««:. 

paring lead concentrations in inhaled and exlwilrd «lr. Thl? was seen a* a tiprftil 

check on the conclusions of the work with radioactive aerosols. As it turned out, 

considerable effort was required to correlate the results of the laboratory (radioactive lead) and environmental (stable lead) measurements, and integration of the 

results into a coherent picture has proved difficult. 

2.2 Previous publications 

The results of the first phase of the project were published (Chamberlain, et al. 

1975). The abstract of the paper was as follows 

-12-
P.14 

"Tetraethyl lead was labelled vtith Pb, added to petrol, and burnt 

in an engine. The exhaust aerosol -vas inhaled by volunteer*, usually 

after it had been stored in a box, but in a few experiments directly, a 

few metres downwind of the engine. The percentage deposition in the 

lung, uptake to blood and excretion of the labelled lead were measured. 

The percentage deposition in the lung depended on the length of 

the respiratory cycle 

-MBS 35 i 2 (s.e.)%. 

half-life of about 6 h. About half of the amount deposited in the lung 

For a 4 s cycle (15 breaths/min) the deposition 

203 Most of the Pb was ronoved from the lung with a 

was in the blood at 50 h after inhalation. A similar fraction was in 

203 the blood at the same time after injection of PbCl_ in saline solution. 

203 

From this and other evidence it is deduced that most of the Pb passed 

from the lung to the blood plasma. About half was removed to bone and 

other tissues, and half became attached to red cells. From about 72 h 

203 onwards, the amount of Pb in blood declined with a mean biological 

half-life of 16 d. Assuming that the same half-life applies beyond 

the period for which measurements were made, the results can be used to 

predict that continuous (24 h/d) exposure to 1 ug/m of exhaust lead 

over a period of months will give an average contribution of about 

1 ug/100 ml to blood lead. Results of other work on experimental and 

industrial exposure of persons to lead in air appear consistent with 

this." 

A shorter paper covering much the same ground was published in the Postgraduate 

Medical Journal (S±, 790-4). 

A paper (Wells, et al. 1977) was given at the Edinburgh Conference on Inhaled 

Particles in September 1975. This was mainly concerned with the effects on deposition in the lung of varying the respiratory parameters (length or breathing cycle and 

tidal volume). The length of the respiratory cycle was found to be a major factor 

in determining the deposition of the sub-micron exhaust aerosol, for which Brownian 

diffusion is the chief mechanism or transfer to the lung surface. When the deposition of 'wind tunnel' and 'box' aerosols was compared, it was found that the wind 

tunnel aerosol gave higher deposition (40% compared with 14*% at 15 breaths/min). The 

wind tunnel aerosol was prepared by diluting the exhaust rapidly with clean air, thus 

giving a smaller particle size than the aggregated aerosol obtained by storage in the 

box. It was pointed out by Wells et al. that the range of variation in the percentage lung deposition, on various assumptions, would correspond to a four-fold variation 

in the calculated relation between blood lead and air lead. 

2.3 Reasons for environmental measurements 

It was known from earlier work (Lawther et al. 1973) that the primary lead-bearing 

particles emitted from cruising engines were very small (< 0.1 pm diameter), but coagulated with other aerosols in the urban atmosphere. Also, Anerican reports have stated 

that larger particles, In the 1-10 pm size range, are emitted In certain cond 11.1 on* 

such as rapid acceleration and ascent of hills. It was therefore decided to make 

measurements of lead in air (PbA) and particle size spectra In six types of location* 

-IS-
P.15 

(a) alongside a motorway in level country 

(b) alongside a motorway on a steep gradient 

(c) in and near major urban highways 

(d) in urban areas not close to major roads 

(e) in an urban multi-storey car park 

(r) in a rural area. 

The opportunity was taken to measure lung deposition in volunteers inhaling the 

ambient aerosol. This was done in locations (a), (c) and (e) above, where the PbA 

levels were high enough to enable this to be done. 

203 

2.4 Reasons ror Pb inhalation and injection experiments 

The earlier work had demonstrated the dirrerence in lung deposition between 

the wind tunnel and box aerosols. In 1977 a more thorough study or the errect or 

particle size in the range 0.02 to 0.09 um was made. The variation was achieved by 

varying the rapidity or dilution or the exhaust. This study or the errect or physical rorm was in parallel with a study or the ejects of chemical state of the lead. 

In the earlier work irradiation or the exhaust aerosol in sunlight had appeared to 

afreet the rate or clearance rrom the lung. It was considered desirable to extend 

this work. The chemical rorm or exhaust lead is very variable. In the work or 

Kehoe (1961b, 1966) and Grirrin et al. (1975) volunteers were exposed to airborne 

lead generated by burning T.E.L. in propane, giving oxide particles. It was therefore desirable to test whether chemical rorms materially altered the uptake or lead 

particles rrom the lung. 

Another series or experiments was done to measure the uptake by blood, and excre203 tion in urine and reces or Pb given by intravenous injection. There were two main 

objectives. Firstly, the measurements or external gamma radiation following injection, together with similar measurements following inhalation, enabled the transfer or 

203 203 

Pb rrom lung to blood to be assessed. Secondly, measurements or Pb in excreta 

following injection gave urinary and fecal excretion rates. The ratio F Al of endogenous fecal to urinary excretion is a useful parameter to apply to measurements of 

excretion or stable lead. Because or the presence or unabsorbed dietary lead in 

feces, it is dirficult to assess the contribution of endogenous fecal lead except by 

tracer studies. A knowledge of the F_A! ratio is needed to assess the uptake of 

dietary lead from the gut by striking a balance between uptake and excretion. 

2.5 Reasons for ingestion experiments 

The reason for wanting to know the percentage uptake from gut is to enable some 

assessment to be made of the relative contributions or airborne and dietary lead. 

As a contribution to this, a study was made or the uptake by volunteers who took oral 

203 

closes or Pb in soluble (PbCl2) and insoluble (PbS) states. Each subject took 

each type or dose aTter Tasting overnight and again with a standard meal, to establish 

if the uptake of a tracer dose of lead is influenced by the presence of food in the 

gut. 

-14-
3: Environmental measurements 

i 

The objectives or the measurements were as follows 

(a) to determine the physical characteristics of thr lead aerosol, 

(b) to measure the fraction of exhaust lead deposited near to its source; this 

fraction is not available f6r inhalation (unless resuspended by some nechanism) 

but may contribute to ingested lead, 

(c) to measure the percentage deposition of environmental lead in the lungs or 

volunteers. ' 

The monitoring or airborne lead levels was not an objective in itself, but sufficient 

data were collected in the course of this work to be worth reporting and comparing with 

other published work. 

3.I Emission or exhaust lead from vehicles 

The tetra alkyl lead riuid added to petrol is burnt in the engine and most or it 

is exhausted as a Tine particulate aerosol. The quantity or lead consumed by the 

engine depends upon its concentration or Pb in petrol, and the rate or petrol consumption which in turn depends on the size, efficiency, running speed and load of the 

engine. The proportion of exhausted lead which is emitted to the atmosphere depends 

not only upon the age, temperature and physical state or the exhaust system, but also 

upon the manner in which the engine is operated, and may vary from 20% to 300%. For 

example, under conditions or heavy acceleration, lead deposits which have accumulated 

in the exhaust system under idling or steady cruising conditions may be resuspended 

and emitted from the tail pipe. 

After reviewing American literature, Huntzicker et aL (1975) took for purposes of 

calculation 75% emission or lead. Assorting a petrol consumption of 30 mpg, 75% 

emission, and a mean concentration of Pb in petrol of 0.49 g 1 , the emission of Pb 

is 56 mg per mile. Measurements at Warren Spring Laboratory of emissions from a 

1100 cc car gave 46 mg/mile at 50 mph, 61 mg/mile at 60 mph and 82 mg/mile at 70 mph 

(Hogbin and Bevan, 1976). The increase with speed is due partly to increased fuel 

consumption and partly to increased percentage emission at high speeds. 

If 1000 cars/hr pass along a road, and each emits 61 mg/mile, then the total 

emission is 16.9 ings" per mile of road or 10 ug m~ s~ . This figure has been 

adopted by Chamberlain, et al. (1978) in calculations of the theoretical concentration 

of lead in air downwind or a road. Little and Wirren (1978) in work on deposition 

near the M4 motorway, adopted the slightly lower figure or 7.7 ug »" s~ , corresponding to 60% emission with the other factors as above. 

3.2 Deposition of lead near roads 

The subsequent fate of Pb emitted to the atmosphere determines the routes of Pb 

uptake by man. It is important to know how much Pb emitted by cars is deposited in 

the near vicinity of a busy road and how much remains airborne and may be Inhaled. 

For this study, a section of the M4 motorway was chosen between Junctions 2 and 3 at 

Heston, London, where it carries about 90,000 vehicles per day (Fig. 3.1). To the 

-IS-
P.17 

north, Va land is permanent pasture and to the south rough grassland. IT deposition 

or parti -s is measured with deposit gauges there remains the problem or relating 

the catch in the gauge to true deposition to the plant and soil surraces. Littl e and 

203 Wirren (1977) have measured deposition or Pb-labelled exhaust to plant and soil 

surraces in a wind tunnel. The deposition velocity defined by 

g 

203 2 

Pb deposited per cm of ground surface per sec 

Concentration of Pb per cm or air 

was 4 times greater to short grass and underlying soil than to bare soil by itseir. 

This was because leaves are erricient in capturing small particles. Consequently 

direct measurements or the Pb content or trays or grass berore and arter a period or 

exposure beside the motorway were made (Little and Wirren, 1978). 

The results or one experiment are shown in Fig. 3.2. The rates oT deposition 

varied considerably on dirrerent days, largely because the wind speed varied. The 

results or Little and Wirren are compared in Table 3.1 with other measurements or 

deposition or Pb near roads and also near smelters. The deposition beside the M4 is 

consistent with other data reported ror roadside sites. Comparison with smelter 

sites shows that although Pb deposition rates are heavy beside the M4 as in the 

vicinity or smelters, the zone arfected by heavy deposition from the M4 is narrow. 

only extending to about 30-50 m rrom the motorway. Roberts et al. (1974) 

-2 -1 -2- 1 

considered that deposition rates or more than 100 mg m month (3.3 mg m d ) 

were excessive Tor residential areas, a criterion adopted by the Canadian Board or 

Health and Ministry' or Environment. In the present study, this level was not exceeded 

beyond 15 m rrom the motorway, even during periods when the wind was blowing in that 

direction rrom the motorway. 

3.3 Comparison or rates or emission and deposition oT lead 

Little and Wirren (1978) calculated the proportion or the lead emitted rrom 

vehicles on a motorway which is deposited within 100 m, using the results described 

in the previous paragraph. The results indicated that only about 10% oT Pb emitted 

under steady cruise conditions on a level motorway is deposited within 100 m or the 

motorway, about 90 % renaining airborne ror long range dispersal. ThereTore the 

decline in concentration or lead in air with distance from the motorway illustrated in 

Fig. 3.2 is due only in small degree to deposition. The main factor is upward dispersion of the plume. Huntzicker et al. (1975) using average Pb emission data for 

Los Angeles, calculated that only about 6% of the calculated emission was deposited 

within 150 m or a busy freeway. The possibility of direct deposition or large 

particles to the motorway surface has been considered (Little and Wirren, 1977), but 

particle size analysis showed that even within 1.5 m of the trarfic less than 10% or 

the mass or lead was associated with particles or 5 pm or greater. At motorway 

access points, roundabouts and trarric lights where especially heavy acceleration 

occurs, there may be a higher percentage or larger particles (Habibi, 1973; Huntzicker 

et al. 1975) and the percentage deposition close to the road may be greater. 

As an alternative approach to this question, Little and WifTon (1978) measured 

• 16-
P.18 

the total Pb content of soils and vegetation in transects out to 100 m from the 

Motorway, and compared the total depc.-'t with the calculated total Pb emission since 

the opening of the motorway in 1965. The concentrations in vegetation and soils at 

100 m were taken as representing the general background levels of urban contamination 

and were subtracted rrom the concentrations measured closer to the motorway to arrive 

at the excess attributable to the total emission. The results Indicated that about 

4 0% or the Pb emitted over the past 11 years has been deposited within 100 m, compared 

with the figure of 10% derived from measuring the current deposition. 

The reason for this difTerence is not known for certain. It is possible that 

deposition is greater during rainfall, but rain falls for only about 10% of the time, 

and even with the unlikely assumption that during rain all the lead was deposited 

within 100 m, that would increase the time-averaged deposition only from 10 to 20%. 

Another more likely reason for the discrepancy is the re-suspension of lead from the 

road surface especially when it is wet. This may include lead in oil which has 

fallen on the road as well as exhaust lead (Little and Wiffen, 1978). 

In dry conditions, there appears to be little re-suspension of lead from roads 

with the normal surface, since electron microscope studies and particle size analysis 

have failed to demonstrate association of lead with re-suspended dust. 

3.4 The possible use of shelter belts for limiting dispersal of lead 

The possible use of hedges or belts of trees for increasing particle deposition 

close to emission sources and for limiting the dispersion of pollution has attracted 

attention. The studies of Impens et al. (1972), Keller (1974), and Heichel and 

Hankin (1976) have all demonstrated that interception of exhaust Pb by hedges or trees 

may be very efficient and that Pb deposition close to a motorway can be greatly 

increased by planting trees. Heichel and Hankin (1976) for example demonstrated that 

accumulation of Pb in soil under a roadside' coniferous windbreak was twice that of 

open ground outside the windbreak. 

Although the presence or trees may increase the rate of Pb deposition close to a 

motorway, the actual quantity deposited may be quite small in relation to the emission 

source. For example, the long and short-term deposition rates to grass and soil 

between 5 and 30 m of the M4 were only 4.5 and 2.0% respectively of the total Pb 

emitted. Even if these deposition rates were doubled by the planting of a belt of 

trees between 5 and 30 m from the motorway as observed by Heichel and Hankin (1976), 

the increased deposition would still represent less than 10% of that emitted. 

3.5 Concentrations of lead in air 

The concentration of airborne lead depends on the distance from the roadway, 

traffic density, driving mode and petrol consumption, wind speed and direction, 

surrounding topography, and on the atmospheric stability which detennines the upward 

dispersion or near-ground sources or pollution. Measurements of airborne lead were 

made in the course of the investigations of deposition near the M4 motorway (Little 

and Wirren, 1978) and also as part of a study of the retention of airborne lead In thc 

lung, described below. In addition, some measurements were made of the urban and 

rural background concentrations. 

-17-
P.19 

The airborne Pb concent rat ions were monitored with air filte r samples (Whatman 

CF/A) normally at a height of 0.3 m above ground. Ttie lead was measured by atonii<: 

absorption spectrophotometry (AAS). The filte r background was 0.2 Mg, so that with 

one-hour sampling at 10 l/min, a minimum lead concentration of 1.3 pg m~ could be 

measured, and with 24-hour sampling, the limit was 0.06 pg m . 

An attempt was made to relate these measurements and others reported in the 

literature, to the trarfic flows where these were known. 

(a) Roadside measurements 

Measurements have been reported by Littl e and WifTen (1978) from a level 

Stretch or the M4 at Heston, Middlesex (Fig. 3.1) and from a stretch of the M40 

where i t ascends the Chiltern escarpment partly on embankment and partly in 

cutting, with an average gradient or 1 in 25 over a distance or 2.5 km (Fig. 3.3). 

The result or one experiment is shown in Fig. 3.2, and the mean results, normalised to a trarric flow of 1000 cars/hr, are summarised in Table 3.2. On the 

M4 the upwind cemcentration was about 0.4 ug/m , which is a typical background 

level for the area. This has been subtracted from measurements on the downwind 

hard shoulder in calculating the normalised concentrations per 1000 petrol driven 

vehicles per hour. Earlier measurements by Bevan e t al. (1974) of concentrations 

in the central reservation or the M4 at Heston are also summarised in Table 3.1. 

The theoretical result X =

 3

»

3

 Mg m~ per lOOO Vh~ was calculated by Chamberlain 

et al. (1976) using Pasquill's (1974) theory or dirfusion or smoke from line 

sources. Average meteorological conditions with wind speed 2 m s~ at 1 m above 

ground were assumed. Theory indicates that the inclination of the wind to the 

motorway does not greatly affect the result unless i t is nearly parallel to the 

road, in which case x is increased. For comparison with long term measurements 

beside roads, a reduction by a factor of 1.5 to 2 would be needed to allow for 

winds blowing both ways across the road. 

The values of x beside the heavily graded M40 are higher than those beside 

the M4, mainly because more fuel is used on the gradient. Where the M40 runs 

in a cutting, poor dispersion increases the concentration further. Comparatively high concentrations of lead (averaging 5.3 pg m* ) had previously been 

observed by Lawther et al. (1973) adjacent to a graded street in Hampstead. The 

trafric flow is not given by the authors, but vehicle counts in the street in 

Hampstead in 1972 (kindly made available by Mr. P.W. Munt) indicate that the . 

24-hour average flow was about 1200 vehicles/hr, with a very high proportion or 

petrol driven vehicles. Assuming a local background or 0.4 Mg m~ , x equals 

4.1 ug m~ per lOOO Vh" at this location. Also shown in Table 3.2 are measurements by Harrison et al. (1974) or airborne lead and trarric flow in London 

streets. Talgarth Road is the link between the Haiimersmith flyover and Cromwell 

Road and the trafric flow and Pb concentration compare with those on the M4. In 

the present work, measurements were made at the Hogarth roundabout in Chiswick 

(A4/A316) where the trarric from the M4 enters urban London (Fig. 3.4). Tlie 

mean concentration in daytime samples one metre from tlie kerb was l<) tm m . 

-18 -
P.20 

The traffic flow between lOOO and 1500 hours was between 4500 and 5500 ,-s/hr. 

In a nearby street about JO m downwind of the roundabout, concentration. craglng 

-3 -3 

4 ug m were found. The daytime concentrations of 3 to 4 ug m rot: \v 

Harrison et al. In West End streets may be compared with daytime metsu .. ;ent* or 

6.4 ug m" in Fleet Street, 2.3 ug m" In Clerkenwell Road and I.S pg a" at 

St.Bartholomew's Hospital by Lawther et al. (1973) 

Lawther e t al. give mean daytime and mean 24-hour levels in London, and the 

Department or the Environment (1976) give mean daytime and nighttime levels in 

Birmingham. Bevan et al. (1974) give the diurnal variation or concentration 

on the M4. Where concentrations are related to local trarric density, the 

24-hour mean can be expected to be a factor 1.2 to 1.5 lower than the daytime 

mean. Where advection from a distance contributes a high proportion of the 

concentration, there is often littl e difference between day and nighttime values. 

At the bottom of Table 3.2, the results of two statistica l correlations of 

urban kerbside lead concentrations and traffic flow are given. These relate to 

long-term measurements with winds blowing both to and from the roadways, and the 

vehicle counts are total, not petrol-driven only. In London, the proportion of 

diesel vehicles is usually about 25%, and assuming this proportion, the result 

of Muskett (1978) is equivalent to x = 2 ug uT per 1000 petrol-driven vehicles 

per hour. The results of Table 3.2 are reasonably concordant. The normalised 

concentration x Per 1000 vehicles per hour at level and not badly constricted 

sites, is about 3 ug m~ when downwind measurements are made, and about 2 Mg m~ 

in long-term measurements. At graded and constricted site s X is increased and 

may be as high as 10 ug nf" . 

(b) Measurements in cars 

Bevan et al. (19 74) found 15 pg/m inside a car with closed windows which 

was driven to and fro between junctions 3 and 4 on the M4 motorway from i100 to 

1500 hours on 5.10.77. The concentration was 76% of the concentration in the 

central reservation at the time. A number of carborne measurements were 

obtained in the present work, and the results are summarised in Table 3.3. All 

the surveys were done in the early afternoon. 

(c) Variation of airborne lead with distance from road 

Tables 3.2 and 3.3 show that concentrations of 10-15 pg m~ can be found 

on motorways, and concentrations of about 5 ug m in very busy streets in 

London. It is important to consider how rar the zone of high lead concentrations 

extends on either side of a busy road. 

Fig. 3.5 shows the concentration gradient with distance from the edge of 

the roadway. The calculations of Chamberlain et al. (1978) took into account 

the effects of vertical dispersion in average meteorological conditions, but made 

no allowance for loss of Pb by deposition. The experimental points or Bevan 

e t al. (1974), Hogbin and Bevan (1976) and Little and Wiffen (1978) are derived 

from surveys beside the M4. A local background of 0.4 ug m~S has been deducted 

-19-
P.21 

fron. u.e insured concentrate, v....; bofc-re repressing them on a percentage of the 

value at tne road (central r«c ir-.-'.tion ;'or Bevan et al. and Hoghin and Bevan. 

hard shoulder for Littl e and Wiffen). Hickman (1976) measured concent ration-» 

in the Cromwell Road and at site s down a side road, 20, 30 and 50 m away. The 

concentrations were 4.1 , 3.0, 2.5 and 1.2 ug m" respectively. Assuming a 

background of 0.6 ug m~ , the decline in concentration with distance is similar 

to that in Fig. 3.5, but the results have not been included as the sampling at 

the 4 site s was not simultaneous. Waller et al. (1965) found average yearly 

concentrations in 1962-3 of 3.2 ug m~ in Fleet Street, 0.8 ug m" in Mitre Court 

46 m away, and 0.8 ug m" also at St.Bartholomew's Medical College, which is not 

near to a major road. Thus the excess concentration from Fleet Street trafric 

was inappreciable at Mitre Court. 

Assuming rrom the consensus or results in Table 3.2 that the long-term 

average normalised concentration x at the kerb or a leve l road is 2 pg m* per 

1000 petrol-driven vehicles per hour, and using the theoretical decline or x with 

distance in Fig. 3.5, the width or the strip on either side in which the contribution to airborne Pb exceeds 1 ug m~ is about 15 m ror a How or 1000 Vh" , 

50 m for 2000 Vh" and 100 m for 4000 Vh" , all expressed as 24-hour average 

flows. There is likely to be considerable variation according to the local 

topography. Hogbin and Bevan (1976) measured lead concentrations in houses near 

the M4 where the trafric averages nearly 4000 vehicles/hr. In continuous 14-day 

samples, 4.8 ug m~ was round inside a bungalow 34 m from the edge beam of the 

motorway. A daytime concentration of 3.0 ug m~ was found in a house at similar 

distance in the present work, compared with 5.0 pg m~ outside the house. However, in a house at 58 m designed with no opening windows facing the motorway, 

Hogbin and Bevan found only 1.1 ug m~ . In a house immediately adjacent to an 

elevated section of the M6 in Birmingham (about 2000 petrol-driven vehicles per 

hour), the concentration was 0.69 ug m~ , and in another with double glazing it 

was 0.44 ug m~ (Department of the Environment, 1978). Ttie level inside both 

houses was 60 to 70% of that outside. The elevation or the motorways in this 

part or Birmingham assists in the electiv e dispersion or exhaust. At the other 

extreme, Lawther e t al. (1973) found 3.7 pg m~ inside a house adjoining a graded 

road constricted by buildings and carrying about 1200 petrol-driven vehicles 

per hour. 

(d) Urban and suburban site s not adjacent to main roads 

Measurements were made at Chelsea College, London, at a distance of about 

100 m from each of 3 main roads. Two sampling positions were used, one at 

ground level and the other on the roof at 25 m. The results are summarised in 

Table 3.4. There was only slightly less Pb in air at 25 m compared with ground 

level, indicating that emissions over a large area accounted Tor the concentrations. On two foggy days concentrations rose to 1.6 ug nf . During the week, 

nighttime concentrations (23.00 - 07.00 h) averaged about 65% of daytime levels 

(07.00 - 23.00 hr), but at the weekends, nighttime concentrations exceeded daytirfe levels by a factor of 1.3. These results may in part reflect recreational 

-20 -
P.22 

population movements within London. Measurements were also made in residential 

areas of Reading (population 132,000) and Didcot (11,000), (Table 3.4). In 

Didcot, the concentrations were strongly affected by wind direction (Fig. 3.9). 

The higher concentrations associated with wind from easterly quarters suggests 

long range transport of lead from the greater London area, with a time delay in 

transport resulting in higher nighttime concentrations. With the cleaner 

westerly airstream, nighttime concentrations were lower than daytime levels 

Indicating greater importance of local lead sources. 

(e) Enclosed car park 

As an example of a specialised situation, measurements of daytime Pb concentrations were made in a poorly ventilated multi-storey car park. Concentra-

-3 

tions varied widely between 12 and 40 ug m according to the degree of ventilation and the volixne of traffic entering and leaving the car park. Most members 

of the public are exposed to these concentrations for only a few minutes whilst 

parking and driving away their cars. 

Measurements were also made of the levels of 00 in the car park using a 

Miran III infra-red gas analyser and Draeger tubes. Daytime levels varied 

between 50 and 300 ppm. Organic lead vapour was also measured using the method 

of Hancock and Slater (1975). Levels of 1.5 and 5.4 ug m~ organic lead vapour 

were measured on two occasions. Purdue et al. (1973) found organic lead concentrations of 1.8 - 2.2 ug m~ in an underground car park. In the present study 

the organic Pb represented 10.0 and 12.8% of the total inorganic particulate and 

organic Pb. These percentages compare with the 15-18% observed by Purdue et al. 

(1973). For a number of open air locations in London, Harrison et al. (1974) 

found values between 0.1 and 4.0%, rising to 9.7% adjacent to petrol-filling 

stations. 

3.6 Particle size analyses 

(a) Objectives and methods 

The particle sizes of ambient lead aerosols were analysed in order to 

(i) ensure that inhalation experiments with artificially generated Pb 

aerosols were representative of lead exhaust aerosols in the environment. 

(ii) correlate the results or inhalation experiments on the ambient 

aerosol In various locations, described in the following secUon. 

(iii) see If more than one source contributed to the aerosol, for exanple, 

re-suspended dust. 

The methods of analysis fall into two groups. Impaction and diffusionbattery devices separate the aerosol into fractions which may be analysed for 

lead. The particle size spectrum has then to be deduced from the characteristics 

of the sampling device. The result refers to the lead-carrying particles. 

Optical methods are more exact but more tedious. A large number of particles 

has to be sized from micrographs. As it is not usually possible to distinguish 

-21 -
P.23 

the lead-tearing particles with certainty, optical methods give the particle 

size spectrum of all particles. 

Andersen impactor samplers have 8 impaction plates and a backing filter. 

The aerodynamic equivalent particle size (50% cut-ofr) is 0.3 pm on the final 

plate and smaller particles penetrate to the filter. Results obtained with 

Andersen samplers are usually plotted on logarithmic probability paper. If the 

logarithms of the particle diameters are normally distributed, the plot comes 

out as a straight line. The mass median equivalent aerodynamic diameter (MMED) 

is then read orr from the plot. If a considerable fraction of the particles 

penetrates to the backing filter, as occurs with lead exhaust aerosols, this 

procedure may fail to reveal that the distribution is not logarithmically normal, 

but is bimodal, with two separate populations of particles. This is often found 

to be the case with ambient aerosols. Whitby et al. (1975) using an electrical 

particle analyser found that fresh freeway aerosol sampled at 30 m was mostly 

below 0.15 pm in diameter. In the present work, about 67% of the Pb in motorway 

samples penetrated to the backing filter of the Andersen sampler. Thus it is 

apparent that aerosol sampled near to rapidly moving vehicles is too fine to be 

characterised adequately by impaction samplers. 

The diffusion battery is a chamber with parallel plates at a separation of 

0.8 mm through which the aerosol is passed. The concentration of lead in the 

air is measured before and after passage through the battery-, and the ratio of 

concentration used to deduce a mean particle size by the method of Metnieks and 

Pollak (1959). The result is called the difrusional mean equivalent diameter 

(DMED). As the Brownian dirrusivity or a particle depends on size and shape 

but not on density, the particle size determined from the diffusion battery can 

be compared with the optical size. 

A thermal precipitator was used to sample aerosols for electron microscopy, 

the particles being deposited directly onto an electron microscope grid. The 

particles on the micrographs were sized in terms of the Feret diameter (the 

distance between tangents at the extremities of the particle perpendicular to a 

fixed direction). 

(b) Motorway aerosols 

The particle size spectrun of a'rborne Pb beside the M4 as measured with the 

Andersen sampler, is shown in Table 3.5. Very little Pb was associated with 

particles greater than 5 pm, although the work or Habibi (1973) suggested that 

a substantial proportion or emitted Pb was greater than 5 pm. The Andersen 

sampler does not operate isokinetically, and was possibly failing to sample the 

larger particles. Placing it with the entry port facing into the wind, so that 

any large particles would tend to be over-estimated, made no difference to the 

percentage of Pb associated with particles greater than 5 pm. A further check 

on large particles was made using a cascade centripeter (Hounam and Sherwood, 

1965). Again, not more than 10% of the airborne lead was associated with 

particles exceeding about 2 pm diameter, with about 90% of the lead being 

-22-
, collected by the final stage of the centripeter. A fraction of the 33% of 

airborne Pb sampled near the M4 which was found on the impaction stages is 

attributable to diffusional deposition of very fine material well below the 

minimum size for impaction. Clearly, the impactor results also indicate a mass 

median equivalent diameter of less than 0.3 pm beside the motorways. Melton 

et al. (1973) and Moran et al. (1972) also found that 69 and 66% of the exhaust 

particles were less than 0.3 pm diameter under steady cruise conditions. 

Electron micrographs of the aerosol as sampled beside the M4 are shown in 

Fig. 3.6. Three types of particles can be distinguished as categorised in 

Table 3.6. The primary particles on the electron micrographs are discrete, 

compact and very electron dense, so that even at the 60,000 * magnification 

required they could be sized readily - category 1. Categories 2 and 3 with 

their much lower frequency were examined at 8,000 x and 2,000 x respectively. 

In Fig. 3.7 a particle size spectrum obtained by visual examination of 

particles is shown. The ordinate is the incremental number of particles per 

cm of air per increment in log radius. 

Similar size distributions were obtained by the M40, the size distribution 

remaining substantially unaffected by the incline. The appearance of the 

aerosol in the electron micrographs suggested that the smallest category carried 

most of the lead. This was confirmed by comparing the volumetric-mean-diameter 

(VMD) of this category determined visually from the number-size distribution with 

the mean diameter deduced from the diffusion battery results. This is shown in 

Table 3.7. With one exception (run of 16.9.76) the two estimates of VMD are 

compatible. Results obtained with the diffusion battery indicated a AMD of 

about 0.03 pm for both the M4 and M40 motorways. Wilson et al. (1977) used an 

electrical aerosol analyser for studying car exhaust emissions on a test trad:. 

They also found three principal categories of particles, these in the "nuclei 

mode" (geometric mean diameter 0.018 pm), the "accumulation mode" (0.21 pm) and 

"coarse particle mode" (4.9 pm). They observed that cars driven at normal 

speeds emit aerosols mainly in the "nuclei mode", and that coagulation within 

these aerosols and coagulation with other aerosols transfers these particles to 

the "accumulation mode". The finding that lead near motorways is mostly in the 

"nuclei mode" has important implications for the rate of deposition on surfaces 

and the uptake in the lung. 

(c) Urban, suburban and rural areas 

When cars are subjected to urban driving schedules on dynamometers, a marked 

shift toward larger particle sizes occurs (see for example Moran et al. 1972, 

Habibi 1973). In the present study, measurements of particle size were made 

beside the Hogarth roundabout at Chiswick to observe the effect of periods of 

heavy acceleration on the emissions of particles in the coarse particle mode. 

The Andersen impactor results showed an increase of the percentages of Pb 

associated with particles in both the accumulation and coarse particle modes, 

with only 30% penetrating to the filter stage compared with 67% on the M4. 

-23-
P.25 

Beside the roundabout, a new peak in the particle size distribution *«s evident 

with 4?% or the Pb between 1.0 and 4.2 Mm aerodynamic Jiar?.. t••r (Table 3.5). It 

is not possible to use the diffusion battery meaningfully ..lien there are many 

large particles, unless these are removed first. Consequently, the Andersen 

impactor was modified to act as a "pre-impactor" with the backing filter 

replaced by a diffusion battery run in series with the impactor stages. The 

diffusion battery revealed a mean diameter of 0.054 um for the 30% of the Pb 

which was less than 0.3 um and penetrated the Andersen impactor. An overall 

mass median equivalent diameter (MrtED) of about 2.0 um is indicated beside the 

roundabout, compared with 0.03 - 0.04 pm by the M4. Thermal precipitator 

samples were also taken for examination by electron microscopy. Fig. 3.8 contrasts the aerosol particle size spectrum with that of the M4. Both Figs. 3.7 

and 3.8 refer to all particles in the aerosol, not solely lead-bearing particles. 

The decrease in number of particles in the nuclei mode, and increases in the 

accumulation and coarse particle modes beside the roundabout, are evident. 

Carbome measurements with Andersen impactors along the North and South Circular 

roads and around major streets in Hammersmith and Chiswick gave a particle size 

distribution intermediate between those of the M4 and the roundabout (Table 3.5). 

The "vMED was about 0.3 pm with 51% of the Pb associated with particles or less 

than 0.3 pm. The peak between 1 and 4 pm observed by the rewndabout was still 

evident, but much less marked (25!%), with slightly higher percentages in the 

accumulation mode (0.3 - 1 um) than found on the motorway. A similar size distribution was observed in the streets of Reading. These Observations are 

similar to those of Cholak et al. (1968), Robinson and Ludwig (1967), and Lee 

et al. (1971), who used impactors in urban situations and demonstrated MvtED of 

Pb aerosols or 0.3 pm, 0.25 pm and 0.18 pm respectively. Biggins and Harrison 

(1978) obtained somewhat larger MMEDs or 0.7 and 0.8 pm with Andersen samplers 

at various locations in Lancaster and Preston, a size intermediate between the 

busy urban and roundabout samples or the present study. 

Particle size measurements with Andersen impactors were also nede at 

Chelsea College, and at County Hall, Westminster, where the Pb aerosol is 

probably typical or large areas or London beyond the immediate influence of the 

nearby streets. No significant differences were observed in particle sizes 

between the roof and ground-level sites at either location. As in the London 

streets, the »WED was about 0.3 um, with 57% penetrating u> !.»••• Uwk.uy, l'U*«-i 

during the sunmer and 51% during the autumn (Table 3.5). For thc periods of 

sampling, this seasonal difTerence was not signiricant. The overall size distribution was very similar to that or the London streets, with the peak in large 

particles observed beside the roundabout again being absent. Under foggy conditions in October, however, only 40% of the Pb penetrated to the backing paper and 

the very slight peak around 1 pm noted in both summer and autumn samples became 

a much broader peak with 48% of the Pb between 0.3 and 2 pm aerodynamic diameter. 

This may have been caused by hygroscopic growth of particles or to greater aggregation in the poorly dispersive conditions. Even in dry conditions, using a 

-24-
P.26 

^irfusion battery An series with an Andersen impactor as a pre-lmpactor, the 

diffusion mean diameter of the Pb particles penetrating the Andersen impactor 

was 0.064 i 0.02 pm, suggesting some aggregation of the finest exhaust particles. 

The aerosol at Qielsea College probably has a complex structure of both fresh and 

aged exhaust components which have been emitted under a wide range of driving 

conditions and have undergone varying degrees of aggregation and deposition. 

In the house, 50 m from the M4, using the difrusion battery without the Andersen 

pre-lmpactor gave a diffusion mean diameter of 0.07 pm compared with 0.03 pm on 

the hard shoulder, again suggesting aggregation and attachment of the 0.03 pm 

primary exhaust particles and transfer of Pb from the "nuclei mode" to the 

"accumulation mode". However, diffusional deposition of the smallest particles 

around doors and windows may have caused some of the depletion of the smallest 

particles inside the house. 

As an exanple of a mature aged aerosol, particle size measurements were 

also made in rural Oxfordshire (Table 3.5). This aerosol was very similar to 

that found at Chelsea College in fog, with 37% penetrating the Andersen impactor, 

and a broad peak between 0.3 and 1.0 pm. This probably represents aggregation 

and attachment of primary exhaust Pb to the ambient aerosol. 

These dirrerences in particle size are relevant to the rates or Pb deposition since the velocity or deposition or particles reaches a minimum between 

0.2 and 0.5 pm and increases steeply with both increasing and decreasing particle 

size (Little and Wirren, 1977). This applies not only to deposition to the 

ground surface, but also to the deposition of Pb in the lungs following 

inhalation. 

(d) Enclosed car park 

The particle size distribution of a concentrated aerosol of medium age from 

vehicles in an enclosed car park was also measured with Andersen impactors and 

diffusion batteries, and by electron microscopy of thermal precipitator samples. 

Andersen samples again showed about 50% penetration, giving a &MED of about 

0.3 pm similar to urban London (Table 3.5). Use of the diTfusion battery in 

series with the Andersen impactor showed a diffusion mean diameter of 0.08 pm 

for the Pb particles penetrating the Andersen. Thus, the particle size distribution was similar to that observed for the urban London street aerosols, with 

some degree of aggregation of primary exhaust and transfer from the "nuclei" to 

the "accumulation" mode. 

3.7 Chemical composition of exhaust lead 

One of the problems in the chemical characterisation or exhaust Pb is that 

changes occur aTter emission to the atmosphere. A further problem is that the small 

size of the particles precludes effective use of electron microprobe techniques. 

Most studies however have reported complex mixtures of lead oxides, halides and 

ammonium salts, together with sulphates and carbonaceous material (e.g. Habibi, l'»73). 

Some of the most recent British work by Biggins and Harrison (1978), using X-ray 

powder diffraction indicates the persistent present of (NH4)2S04. PbS0>4, together 

-25-
P.27 

with lesser amounts of PbS04 and PbBrCl. They believe that (NH4)2S04.PbS04 is an 

intermediate in the conversion of vehicle-emitted lead halides to PbS04, formed by 

reaction with atmospheric ammonia and acid sulphates. The solubility of the compound is intermediate between that of the sparingly soluble oxides and the more 

soluble halides and nitrates. On account of its small particle size it is likely 

203 to be readily soluble in the lung, since inhalation experiments with PbO aerosols 

showed rapid uptake of Pb from the lung into the blood stream (see Section 6 below). 

In the present study a continuous flow solubility technique using aerosol particulates collected on 'absolute' filters has shown that the lead associated with motor 

exhaust aerosol, whether fresh or aged, is extremely soluble in distilled water at 

20 C. Under similar conditions the lead associated with lead oxide aerosols 

dissolves much more slowly. 

For example, for motor exhaust lead 92% dissolved in 1 ml water flowing for 2 

minutes whereas for lead oxide only 11% dissolved in 40 ml water flowing for 90 

minutes. 

Increasing the temperature to blood-heat (37 C) and using blood plasma as the 

solvent raised to 19% the lead dissolving in 90 minutes from the lead oxide aerosol. 

-26-
I 

TABLE 3.1 

Lead deposition rates at various locations 

Location 

Rural site s U.K. 

Urban site s 

Pasadena 

San Diego 

Palo Alto 

Cincinnati 

New York 

Chicago (airport) 

London, Heston (semi-rural) 

Smelter site s 

El Paso (0.1 km) 

Toronto (0.15 km) 

Avonmouth (0.1 km) 

" ( 1.0 km) 

" (3.0 km) 

Roadside site s 

10 m from road with 4,000 vehicles hr~ 

15 m from road (Palo Alto) 

1 m from road with 62,000 cars day"' 

30 m it it II II II II 

150 m " " " " " " 

Central reserve of M4 

0 m from hard shoulder of M4 

5m " " " " " 

15 m " " " " " 

30 m " " " " " 

Pb deposition rate 

(mg nr 2 day- 1 ) 

0.02 - 0.17 

' 

0.45 

0.07 - 0.95 

0.37 

0.35 - 3.2 

0.14 - 1.4 

0.46 

0.2 

7 

18 

5.0 - 11.5 

0.5 - 4.0 

0.4 - 1.0 

3.2 

1.4 

23.0 

1.5 

1.0 

10 - 16 

6-1 5 

2.3 - 6.2 

1.1 - 3.1 

0.6 - 1.8 

Deposition surface 

Deposit gauge 

Deposit gauge 

Deposit gauge 

Pan 

Deposit gauge 

Deposit gauge 

Polythene buckets 

Soil and grass 

Deposit gauges 

~ Deposit gauges 

Deposit gauges 

Deposit gauges 

Deposit gauges 

Sedimentation Jars 

Pan 

Deposit gauge 

Deposit gauge 

Deposit gauge 

Grass and soil . 

Grass and soil 

Grass and soil 

Grass and soil 

Grass and soil 

Reference 

Cawse (1974) 

Huntzicker e t al. (1975) 

Chow (19 70) 

Atkins (1969) 

Cholak e t al. (1968) 

Volchok e t ali (1974) 

Lazrus et al. (1970) 

This work 

Landrigan e t al. (19 75) 

Roberts e t al. (1974) 

Littl e (1974) 

II it 

II II 

Cholak e t al. (1968) 

Atkins (1969) 

Frledlander * Huntzicker (1974) 

it it n 

ti n it 

Littl e S Wiffen (1978) 

•i II •• 

II II n 

n « » 

II II •• 
TABLE 3.2 

Measurements oT lead in air beside motorways and other streets 

f 

Location 

M4 central reservation 

M4, 2 m Trom edge beam 

M40, 2 m frcm edge beam 

leve l 

1/20 grade in 

cuttin g 

l/2 0 grade on 

embankment 

Theoretical result 

London, Flee t Stree t 

Central reservation 

Heath Road, Hampstead 

(on hill ) 

Exhibition Road, S.W.7 

(kerbside ) 

Seymour Place , W.1 

Talgarth Road, W.H 

Upper Berkeley Street, 

W.I 

, Various site s 

; 

Rome, 4 site s 

Open or 

constricte d 

sit e 

0 

0 

0 

C 

0 

0 

C 

C 

0 

C 

1 0 

c 

mm 

-

Sampling 

periods 

24-hour 

Daytime 

n 

II 

n 

II 

Daytime 

24-hour 

Daytime 

i " 

•I 

•I 

24-houi 

Petrol 

Vehicle s 

per hour 

3800 

3600 

970 

950 

990 

-

1200 

1200 

1300 

424 

3880 

420 

Lead in a 

Measured 

15.1 

8 . 9 

3 . 3 

10.3 

6 . 4 

-

3 . 2 

5 . 3 

3 . 2 

4 . 0 

8 . 8 

4 . 3 

1 

• statistica l survey 

(al l vehic l es) 

i r (ug m"- ) 

Background 

(estimated) 

0 . 4 

0 . 4 

0 . 2 

0 . 2 

0 . 2 

-

0 . 8 

0 . 4 

0 . 5 

1.0 

0 . 5 

1.0 

- 3 

pg m per 

1000 Vh-' 

3.9 

2 . 4 

3 . 2 

10.0 

6 . 2 

3 . 3 

2 . 0 

4 . 1 

2 . 0 

7.1 

2 . 2 

7.9 

1.5 

1.8 

References 

Bevan e t al . (1974) 

Littl e and Wifren (1978) 

it ti II II 

II it tt ti 

ii it II it 

Chamberlain e t al . (1978) 

Waller e t al . (1965) 

Lawther e t al . (1973) 

Harrison e t al . (1974) 

it it it 

II it •• 

tt II it 

Muskett (1978) 

Colacino k Lavagninl 

( 1974) 
"TwrT^T m>1fr 

P.30 

TABLE 3.3 

Measurements of airborne lead in carbome surveys 

Location 

M4 between junctions 2 and 5 

North and South Circular roads 

A4 between Chiswick and Hammersmith 

Reading streets 

No. of 

runs 

4 

2 

3 

1 

Pb concentration 

Mg/m3 

11.5 

5.7 

5.2 

2.1 

TABLE 3.4 

Measurement of airborne lead at rixed sites (24-hour results) 

Location 

Chelsea College 

Ground level 

Roor 

Roor 

Roor 

Reading 

Didcot 

London, County Hall 

London, St.Bartholomew's 

Hospital 

Date 

July 1977 

July 1977 

Sept/Oct. 1977 

July 1978 

May 1978 

May 1978 

July 1978 

1975/6, summer 

1975/6, winter 

1971/2 

Pb concentration 

M« m~3 

0.46 

0.39 

0.80 

0.46 

0.35 

0.20 

0.19 

0.50 

1.06 

0.6 

Reference 

This work 

ti it 

n tt 

tt it 

ti it 

it ti 

it ti 

Ball & Hume 

(1977) 

it II 

Lawther et al. 

(1973) 

-29-
P.31 

TABLE 3.5 

Pe-ticl e siz e 

50% cutofr diam. 

um 

11.5 

9 . 5 

5.7 

4 . 2 

2.2 

1.0 

0.5 

0 . 3 

<0.3 

M4ED (um) 

CMED* (pm) 

KWED (pm) 

tMED* (pm) 

i 

1 ! 

t 

i 

i 

1 

1 

fcMED (pm) 

CMED* (um) 

analysis or airborne Pb measured with Andersen J.mpacto 

(Mean percentage on each stage i S.D.) 

M4 

* 

1.59 

1.83 

3.1 0 

4.39 

4.9 5 

4.87 

7.24 

4.7 4 

67.38 

0.0 4 

0.0 3 

S.D. 

0.6 0 

0.34 

0.65 

1.14 

0.67 

1.08 

5.01 

0.99 

2.13 

Chelsea College 

(summer) 

3.72 

2.24 

4.54 

5.34 

5.96 

7.78 

6.7 8 

6.4 0 

57.23 

0.22 

-

2.36 

0.79 

2.01 

1.94 

1.76 

2.35 

4.5 0 

2.27 

7.05 

Rural Oxfordshire 

2.81 

2.46 

3.07 

4.2 0 

6.1 0 

12.37 

14.39 

17.37 

37.23 

0.22 

-

0.59 

0.36 

0.57 

0.64 

1.67 

1.53 

3.1 0 

5.43 

4.36 

Hogarth roundabout 

% 

6.66 

4.61 

6.53 

14.52 

14.16 

13.75 

4.76 

2.59 

30.47 

2 . 0 

S.D. 

0.61 

0.98 

0.61 

0.94 

1.06 

0.59 

0.86 

0.52 

2.52 

0.054 

Chelsea College 

'(autumn) 

2.41 

2.36 

4.24 

4.19 

7.63 

10.02 

6.86 

0.77 

0.69 

0.6 0 

0.83 

1.19 

1.33 

1.94 

8.06 j 2.43 

51.27 ; 5.89 

0 . 3 | 

0.064 

Enclosed car park 

2.71 

2.77 

4.3 0 

7.42 

8.42 

10.60 

5.62 

5.08 

53.19 

0 . 3 

1.04 

0.77 

1.22 

1.90 

1.74 

0.94 

1.62 

2.03 

3.36 

0.08 | 

rs 

London streets 

* 

2.77 

2.77 

3.62 

5.77 

7.75 

11.11 

6.3 2 

9.01 

50.89 

0 . 3 

-

S.D. 

0.61 

0.61 

1.26 

2.14 

1.61 

2.64 

1.10 

4.2 7 

2.44 

Chelsea College 

(fog) 

1.96 

1.38 

3.82 

6.0 5 

10.20 

15.70 

10.38 

11.58 

0.36 

0.45 

0.0 0 

1.03 

1.73 

2.45 

0.56 

1.39 

39.80 8.21 

0 . 5 

" 

Laboratory 

<1.00 

<1.00 

<1.00 

<1.00 

<1.00 

-

i 

-

28.40 - 5.19 

56.16 7.52 j 

13.64 2.71 i 

<1.00 

— 

-

Of the fraction penetrating to the filter stage. 

-30 -
TABLE 3.6 

i 

Categories or particle in electron micrograph* 

Category 

1 

2 

3 

Size 

pm 

<0.1 

0.1-1.0 

0.5-5.0 

Appearance 

Opaque discrete, rounded 

Diaphanous, chain aggregates 

Dense, flaky or amorphous 

Supposed origin 

Primary lead particles 

produced in engine 

Mostly diesel smoke 

Carbonaceous particles 

from tail-pipe or 

adventitious particles 

from distant sources or 

re-suspended from road 

TABLE 3.7 

Volumetric-mean particle diameters 

Motorway 

M4 

M40, incline 

M40, level 

1 

Mean of level 

site s 

Date 

13.10.75 

16.9.75 

17.6.76 

1.7.76 

12.6.76 

8.9.76 

29.10.75 

26.11.75 

13.4.76 

26.5.76 

Particle siz e (um) 

Diffusion battery 

(CMED) 

_ 

0.03 

0.035 

0.03 

0.03 

0.045 

-

-

0.03 

0.03 

0.033 

From electron 

micrographs (VMD) 

0.024 

0.08 

0.052 

0.045 

0.048 

0.042 

0.014 

0.021 

0.020 

0.016 

0.044 

-SI-
"T;-TT»T-7

n|ffTf'• 

~ \ 

^ 

AERE - R 9198 Fig. 3.1 

M4 motorway at Heston 

32 
» 

19 

18 

17 

IS 

IS 

H 

1] 

12 

I I 

10 • 

. 

t 

7 

6 

5 

4 

1 

2 

1 

WINO DIRECTION 

i 

I 

I 

I 

I 

i / 

/ / 

/ / 

.-—^g 

^';-

« 

t 

m 

i 

s 

6 

5m HorO 

rtoulotr 

CwMrol 

(•MTVQtion 

Mora 

»houl<»»r 

Sm 15m 30m 

AERE • R 9198 Pig. 3.2 

Concentrations of Pb In air and rates of Pb deposition to grass across the M4 motorway 

-33 -
AERE - R 9198 Fig. 3.3 

M40 motorway 

- 34 
"Tf* • !••"TT1T" " 

AERE - R 9198 Fig. 3.4 

Hogarth roundabout 

-35 -
P.37 

100 

TO 

In 

**o 

o 

o 

c 

o 

c 

o 

c 

o 

u 

0) 

o 

c 

A) 

O 

tOl 

Q. 

1 0 -

T i r I ' ' ' ' I T—I—i— r 

1 1 

10 50 100 

Distance (m) 

150 

AERE. R9198. FIG. 3.5. VARIATION OF CONCENTRATION WITH DISTANCE 

FROM MOTORWAY. 

x LITTLE & WIFFEN (1978) O BEVAN et al (1974) 

A HOGBIN & BEVAN (1976 ) ERROR BARS ARE 1 S.E. 

THEORETICAL ( CHAMBERLAIN et al 1978 ) 

-36 -
0.1 pm 

1 n..m 4.0 pm 

1.0 pm i r i 

, »•• •, < Tv i''•>•*•"»;,.»*,^ i & 

* " •

 4 '";i-. ,.*. V i , . ;, t ^ *-- . 

'"•>*;• ••••: -v^*>'i*'' ^ 

a, -•-' ,;.'•"•> ' ;•• .- # * •».-» r •*.? 

•« •••».- • • • 'a, ,~ • -a • . -J * _, . 

•*••- • i** ;

 ; v-**^ * • • -•* " •-?•*? 

,•• :.•* x.. vv«. *..-,-••'.;*.',* 

? ^ r - ' : v«- ' •<>*->-»^~ 

-"-•»•••''• .Tr-.-v-'.-"--*'•=*•'•>•> 

. ' a. .-V O.' ^ ... ». .'' l 

! —».-• > .• . mi a- '* • rJf •' 

• . I . ^ * ,*.•• ' -. * . * • am. 

••:•: -• :im.-:::->'-4&'?^rr. r--.---v*-*.-.:---'----*•- « 

% * . • **v 

.V 

2 

Particle categories 

A typical motorway 

AERE - R 9198 Fig. 3.6 

vehicle exhaust aerosol viewed by electron microscopy at three magnifications 
-tp^W yimTaafrJ-"TM! 

106L 

E 

o 

* 

o. 

Ol 

o 

.T3 

10 

10- h10 

10 

10 

iL—L 

10" 

—i r 

M4 HESTON 

Small 

opaque 

spheres 

Carbon 

chain 

aggregates 

Large 

particles 

1 

10 -2 

_L ± 

-1 10 

Diameter ( urn ) 

10 

AERE . R9198. FIG. 3.7. VEHICLE AEROSOLS. SI2E DISTRIBUTIONS 

OF THREE CLASSES OF PARTICLE . 

-38 -
T T * '"•"•^nr1 

• 

10* 

5 

10 

c*> 

£ 

u 

» 4 

o 

o '*•••"• " 

•o 

•J*? 

" io3 

102 

1 

10 

1 

l l | l 

\ 

\ 

'"V T 

-r—[— 

-

— o M4 Mot 

— x Hogarth 

i il l 

°\ 

\ 

orway 

round< 

. 1 

- •* 1 j i • | i 

v 

\ 

\ 

\ N 

\ o Vk 

\ \ 

r? 

V 

\ 

ibout V 

\ 

\ 

•ft 

• \ 

\ \ 

. 1 , 1 1 \ , 

' : 

***** 

_ 

-

_ 

M 

-

•"*" 

-

*~ 

aa 

ma 

1 

0001 001 0 1 1 10 100 

Particle diameter (um ) 

A.E.RE.R9198. FIG. 3.8. TOTAL PARTICLE SIZE DISTRIBUTIONS AT M4 

(HESTON) AND HOGARTH ROUNDABOUT. 

-39 -
t 

0 28 

026 

022 

•a. 

.o 

018 

0-14 

0-10-

0 06 -

• Daytime 07 M-19 M 

x Nighttime 19 M-07° * 

JL l _L 

W NW N NE 

Mean wind direction over 72h periods 

AERE . R9198. FIG. 3.9. LEVELS OF AIRBORNE Pb IN A SMALLTOWN ( DIDCOT. OXON) 

COMPARISON OF DAYTIME AND NIGHTTIME LEVELS AND THE EFFECT OF WIND DIRECTION 

MAY- JULY 1978. 
P.42 

4. Inhalation of stable lead 

4.1 Methods of measurement 

The aim was to measure the deposition of inhaled Pb in the lungs at motorway, 

urban and suburban locations. It was thought that differences in particle size would 

be reflected in percentage deposition in the lung. Ttie method was to measure the 

concentrations in Pb in inhaled and exhaled air, together with the volune breathed, 

and by difference to calculate the deposition of lead in the human subject. The 

subjects inhaled ambient air by mouth via a non-return valve (Figs. 4.1, 4.2). 

Throughout, the nose remained closed with a clip and deposition of Pb in the nose was 

avoided. After filtration, the exhaled air passed through a gas meter to measure the 

volume breathed. The tubing of the apparatus was kept to a minimum to minimise the 

double swept volume and the deposition losses of Pb to the apparatus itself. During 

cold weather the exhalation filters were enclosed in insulated, heated boxes to 

prevent wetting of the filter paper with condensed water vapour. To minimise the 

pressure drop across the exhalation filters it was necessary to use 18 cm diameter 

discs of Whatman GF/A filter papers supported by nylon gauze in specially constructed 

glass holders. By introducing a pressure transducer into the system, linked to a 

chart recorder, a record of breathing was obtained from which mean tidal volune, and 

the duration of breaths, were calculated. . 

The normal method of extracting Pb from small filter papers.was to boil them in 

a few ml of concentrated HNO, in a beaker, or to reflux the papers in 50% HNO,. 

However the large GF/A papers presented certain problems. Since the papers do not 

dissolve in HNO,, and are reduced to a pulp only by vigorous boiling, it was impractical to boil them in a small volume of acid. Furthermore, the reflux "wet-ashing" of 

such a large GF/A paper released about 12 ug Pb even from a blank, unused paper, 

whereas only 6 ug might be collected on the exhalation filter paper during a 3-hour 

inhalation of 10 ug m 

-3 Consequently it was necessary to extract the exhaled Pb 

from the paper without extracting the intrinsic Pb from the paper itself. Various 

203 techniques were appraised using Pb-labelled exhaust. 

Sequential leaching of the papers with cold 0.5% HNO, proved most satisfactory 

resulting in 95% extraction of exhaust Pb from the papers whilst consistently removing 

only 1 Mg of the intrinsic Pb. This extraction procedure was validated with stable 

exhaust Pb by comparing measurements of Pb in air using both small (2 cm) and 18 an 

203 diameter papers in parallel. Previous work with Pb had validated the inhale/exhale 

filter method for measuring human retention of Pb (see Section 4.3 below), and given 

the opportunity to measure Pb deposition to the tubing and valves of the equipment 

Itself. Using stable lead in the field, a signal on the exhalation filter of 2 Mg 

(i.e. 0.2 Mg ml" for AAS) or twice the unused paper background value of 1 Mg was the 

limit of sensitivity of this technique, although a signal of at least 3 Mg was preferred. Thus, in an inhalation experiment with a duration of 41$ hours, the maximum 

possible without undue discomfort to the subjects, 2.0 Mg •»" was the minimum feasible 

concentration of Pb in air (50% retention assumed). 

-41-
P.43 

4.2 Inhalation experiments in the field 

A total of 46 inhalation experiments was done by 3 subjects. The locations 

were 

(a) Motorway - on the hard shoulder of the M4 at Heston (Fig. 4.l), or 

travelling in a vehicle to and fro between Junctions 2 and 5 (Fig. 4.2). 

(b) Roundabout - alongside the Hogarth roundabout at Chiswick. 

(c) General urban - in vehicles travelling in the busiest areas of Chiswick 

and Hammersmith, on the North and South Circular Roads and in Reading. 

(d) Car park - in a multi-storey car park. 

Inhalations were not practicable in suburban or rural areas as a minimum Pb 

-3 concentration of 2 pg m was needed. 

The breathing parameters were not standardised, as it was impracticable to set 

up spirometers and similar equipment on motorway hard shoulders and in moving 

vehicles. Also it was preferred that subjects breathed normally, and they usually 

became unaware of their breathing patterns after a few minutes. the arrangements 

made to minimise resistance to breathing in the apparatus helped in this respect. As 

in laboratory experiments, the percentage deposition in the lung depended on the 

length of the respiratory cycle (Fig. 4.3) which varied between subjects. Variation 

with tidal volume is also to be expected. However analysis of variance of the 

results of Table 4.1, using the method for unequal numbers in sub-classes with one 

missing plot (Kendall, 1945), she-wed that between-subject variance fell just short of 

significance at the 5% level. Between-location variance was significant at the 1% 

level. 

The mean deposition in the lung of 6.1% given in Table 4.1 for the motorway 

203 inhalations is consistent with laboratory results obtained with Pb-labelled fresh 

exhaust aerosol having IMED of 0.03 um (Table 3.7) (see Section 5 below). It was 

not expected that percentage deposition at the roundabout would be equally high as it 

had been anticipated that aggregation would have reduced the proportion of lead in the 

nucleus mode. The fraction penetrating to the filter of the Andersen impactor at the 

roundabout was less than at any of the other locations, where particle sizes were 

measured. The particle size distribution at the roundabout was bimodal, with 30% of 

the Pb having a mean diffusional diameter of 0.05 Mm and 42% being between 1.0 and 

4.2 Mm equivalent diameter. Diffusional deposition of the small fraction would have 

been efficient in the pulmonary region of the lung whilst impaction of the larger 

particles in the tracheobronchial system may have contributed to the high overall 

deposition. If this was so, the assimilation of the deposited Pb may have been 

different at the two locations, with possibly more mucociliary clearance of the 

larger particles at the roundabout. It was not possible to measure the uptake of the 

lead to the blood, aince the elevation of blood lead in any one inhalation can be 

calculated to have been no more than a fraction of 1 Mg per 100.ml of blood. 

The mean values for pulmonary deposition of the general urban and car park lead 

aerosols were both 48%. The particle size distributions were also similar, the 

-42-
P.44 

Andersen impactors giving a *WED of 0.3 Mm, which is a figure often quoted for urban 

lead aerosols in the USA. The percentage penetrating to the filter of the Andei-Arn 

sampler in the urban areas was intermediate between corresponding percentages for the 

M4 and roundabout aerosols (Table 3.5) and the IWED of the penetrating fraction 

(0.08 |*i) was slightly higher than in either of the other two cases. The urban 

aerosols thus lacked the potential for very effective deposition either by diffusion 

or impaction. This may have been true also of the rural aerosol, but no lung 

deposition measurements could be made with it. 

Although the variations of percentage deposition with location in the field 

experiments were explicable in terms of the particle size analyses, the results for 

203-

the urban locations appeared to differ frcm expectation based on the Pb experiments, 

particularly when compared with the results of Wells et al. (1977). In that work 

only 15-20% deposition of aggregated aerosols (0.5 m WVIED) was obtained compared with 

48% deposition of urban and car park aerosols (0.3 um *WEC) in the field. The 

laboratory aerosols were in a narrow size range and lacked both the smallest and 

largest ends of the particle size spectrum found in the field. Nevertheless the 

field values were higher than expected from theory (Mercer, 1975). 

4.3 Comparison of field and laboratory methods 

Since different sets.pf equipment and methods of analysis were used for the 

laboratory and field inhalations it was decided to do laboratory experiments with an 

aggregated non-radioactive aerosol using the field equipment. The results are shown 

in Table 4.2. The observed deposition averaged 55% for subject PL and 42% for 

subject MJH. Using the regression lines of percent deposition versus length of 

respiratory cycle derived by Wells et al. (1977) frcm experiments with aggregated 

203 

Pb aerosol, averages of 22% and 18% deposition would have been expected. It 

appeared therefore that the higher deposition found with stable lead measurements in 

the field applied also when stable lead analysis was applied in a laboratory 

experiment. 

In a further attempt to resolve the discrepancy a more elaborate comparison was 

made using both stable and radioactive lead simultaneously. The original laboratory 

system of cylindrical exhalation filters and spirometer breath control was compared 

with the field system comprising disc exhalation filters, pressure transducer and 

breath recorder, and gas meter. A balloon was added to the latter after the gas 

meter, so that the volume could be confirmed on the standard "wet" gas meter used in 

all laboratory work. Both subjects PL and MJH did two inhalations of each type. 

With the laboratory equipment the tidal volumes were 1.1 and 1.7 1 as in previous 

laboratory work. With the field equipment the breathing patterns were natural and 

were unobserved by the subject. Intermediate inhalations were also done using the 

laboratory equipment with the spirometer replaced by the pressure transducer and 

recorder, and with natural breathing patterns in order to see whether conscious 

regulation of breathing was an important factor. 

Following each inhalation with the field equipment radioactive counting was done 

on all the intact filter papers, and also on the solutions following extraction of the 

-43-
P.45 

paper prior to analysis by AAS. Th* efficiency of Pb recovery from the large 

exhalation disc filters was 99.2% w'-h S.D. 0.2ft. There was good agreement between 

the estimates of percentage deposition from radioactive and stable Pb analysis, the 

ratio of radioactive:AAS measurements being 1.02% with S.D. 0.15 (Table 4.3). In 

addition, rig depositions with the field equipment were checked by radioactive counting and all the figures for percentage retention were corrected for rig deposition 

and double swept volumes. Estimations of the retention of radioactive Pb were also 

cross-checked by whole body counts. 

Measurements of particle size were made using Andersen impactors and the results 

derived by both radioactive counting and AAS. The particle size distributions of 

radioactive and non-radioactive Pb were virtually identical. As in previous laboratory inhalations a stable aggregated aerosol of ftMED 0.5 Mm was observed. 

There was very good agreement between the radioactive and stable Pb analyses, 

validating the extraction and AAS analysis procedures following field inhalations. 

The two sets of equipment also produced quite similar results using the same aerosol, 

although the ratios of observed/calculated values tended to be higher for the field 

equipment than for the laboratory equipment. Whether breathing patterns were 

conscious or not, seemed to make no difference. Both methods produced values for 

percentage retention somewhat higher than the values obtained by Wells et al. (1977) 

and in better agreement with the data from Chamberlain et al. (1975). The reasons 

for the "discrepancies between the three sets of data remain unresolved. 
P.46 

TABLE 4.1 

Deposition in lung of environmental lead 

(a) tidal volume, litres; 

(b) length of respiratory cycle, seconds per breath; 

(c) percentage deposition. 

Subjec t 

A • "L.» W • 

, t 1 

Mean & SE 

M* J •!!• 

1 

1 

, Mean & SE 

;

 P.L. 

1 

i 

\ 

Motorway 

( a ) (b) (c ) 

1.5 6. 0 74 . 

1.2 6. 4 85 

- - 71 

0.6 5.1 58 

72 1 6 

1.4 4. 7 6 3 

1.1 4.6 52 

0.6 4. 3 70 

0.6 5.2 68 

1.0 7.1 57 

0.7 5.5 30 

0 . 8 5.1 48 

0.7 5. 0 62 

0.6 4. 9 53 

56 1 4 

- - 77 

0 . 8 5. 9 68 

0.6 4. 2 42 

0.7 4. 3 55 

0 . 5 4. 2 67 j 

0.6 4. 2 63 1 

Roundabout 

(a) (b) (c ) 

- - 80 

- 57 

0 . 8 6. 3 65 

67 i 7 

- 62 

62 

0 . 9 5.8 67 

0 . 9 5. 2 62 

- 55 

General Urban 

(a) (b) (c ) 

- - 59 

1.0 6. 0 55 

0 . 8 5.6 31 

0 . 7 5.5 46 

- 26 

0 . 7 5. 3 45 

0.6 4. 5 41 

43 i 5 

0 . 6 5.1 28 

• 

28 

1.2 6. 9 70 

- - 68 

- - 47 

- 51 

0 . 8 4. 9 40 

- - 58 

0.6 4. 0 42 

Car park 

(a) (b) (c ) 

' i 

0 . 7 5. 4 47 

0.7 6. 0 37 

0 . 7 5. 0 42 

1 

| 

42 r 3 

0.6 4. 2 66 

0 . 5 4. 1 46 

0.6 4. 4 51 

Mean & SE 

A ll subjects 

62 i 5 

61 * 3 

61 ± 3 ; 

I 1 

6 4 1 j j 

54 1 5 : 

48 1 4 

54 : 6 

48 *: 4 

-45-
''""•*•" '•"-•TTTT" 

TABLE 4.2 

Deposition in lung of stable aggregated exhaust Pb using field equipment 

Subject 

P.L. 

1 

2 

3 

4 

5 

M* J alia 

1 

2 

Tidfaj volume 

(litres) 

0.85 

0.84 

0.96 

1.07 

1.01 

0.76 

0.75 

Seconds 

per breath 

6.1 

6.1 

5.2 

5.5 

5.4 

5.6 

5.7 

% deposition 

Observed 

56.2 

59.1 

48.1 

54.4 

53.9 

41.2 

42.4 

Calculated* 

22.3 

22.3 

21.0 

21.8 

21.5 

17.9 

18.1 

observed 

calculated 

2.61 

2.65 

2.29 

2.50 

2.51 

2.30 

2.34 

* Derived from Wells et al. (1977) with a factor 1.1 to correct for 

MJH from tidal volume of 1.0 1 to 0.76 1. 

TABLE 4.3 

Percentage deposition by radioactive and stable lead analysis 

Subject 

MJH 

PL 

Run 

I 

II 

III 

IV 

V 

I 

II 

III 

IV 

V 

Apparatus 

Cyl. spiro. 

Cyl. spiro 

Cyl. recorder 

Disc.recorder 

Disc.recorder 

Mean & SE 

Disc.recorder 

Cyl. spiro. 

Cyl. spiro. 

Cyl.recorder 

Disc.recorder 

Mean & SE 

Tidal 

volume 

1. 

1.14 

1.77 

1.10 

0.75 

0.80 

1.11 

0.76 

1.14 

1.77 

0.89 

0.75 

1.06 

1 

Sees 

per 

breath 

7.8 

9.9 

5.9 

5.9 

6.3 

7.2 

5.2 

8.9 

10.1 

5.47 

5.47 

7.0 

% Deposition 

Pb2 0 3 

32.3 

43.8 

41.0 

30.1 

30.8 

35.6 

t 2.8 

29.6 

45.5 

55.2 

32.1 

41.7 

40.8 

t 4.6 

Stable 

Pb 

-

-

-

24.2 

32.9 

28.6 

32.1 

42.9 

37.5 

Calculated 

28.4 

37.5 

21.9 

18.5 

18.8 

17,5 

34.8 

45.6 

24.4 

24.5 

Observed 

Calculated 

1.14 

1.17 

1.87 

1.47 

1.69 

1.76 

1.31 

1.21 

1.32 

1.73 

i 

-46-
vm-fjyw- p-=. iryifff. •-

AERE - R 9198 Fig. 4.1 

Subjects inhaling exhaust aerosol on the hardshoulder of the M4 

47 
c 

CM » 

"*' I 

£ ? 

c 

00 o 

°> "5 

O) CD 

c. 

tt .E 

' 0) 

tt o 

UJ XI 

48 -
1 

to 

at 

c 

3 

r 

r 

o 

~ 

M 

O 

a. • 

o 

80 

70 

60 

50 

AO 

30 

20 

10 

mm 

•""T-

' 

—r 

„. i 

I T ~ 

o Motorways 

• Urban 

i i 

" T -

• 

i 

— I 

i 

f 

o 

i 

— , , r 

o 

o ° 

° ° o • 

o 

o 

o ° 

o 

• 

• ° m • • 

• 

1 1 . 1 

i — i r— 

o 

o 

• 

• 

• 

% 

1 1 1 

—.—,

—

 , 

• 

o 

— 

-

-

1 

0-5 1 0 15 2 0 2 5 3 0 3 5 4 0 4 5 5 0 5 5 6 0 6 5 7 0 

Length of respiratory cycle Is.breath"') 

A ERE. R9198. FIG. 4.3. DEPOSITION OFLEAD IN LUNG IN FIELD EXPERIMENTS VERSUS LENGTH OF 

RESPIRATORY CYCLE. 

. o 
5. "Inhalation of radioactive lead aerosols 

5.1 Object of experiments 

a The radioactive labelling of exhaust aerosols was done to enable the deposition 

in the lung, transfer to other organs, and excretion of lead to be followed by 

detection of the radioactive label. In this way, the fate in the body of lead 

inhaled during a short period of exposure could be determined without interference 

from the background of stable lead already present in tissues. Previous .work 

(Chamberlain et al. 1975, Wells et al. 1977) had given considerable information on 

the percentage deposition in the lung and its dependence on tidal volume and length 

of respiratory cycle. In the present work, particular attention was given to fresh 

non-aggregated exhaust aerosol, since work in the environment (Section 3 above) had 

shown that this was the form of the ambient aerosol particularly near motorways. 

Work with aggregated exhaust aerosols, and with lead oxide and nitrate aerosols, had 

the main object of looking for possible effects of chemical composition of the 

particles on the rate of clearance from the lung, but the opportunity was also taken 

to measure percentage deposition. The inhalation pattern in these experiments was 

chosen to maximise deposition in a relatively short inhalation without using unnatural 

breathing patterns. , 

5.2 Preparation and inhalation of labelled aerosols 

203 

The isotope Pb is produced by bombarding thallium with protons in the cyclotron at the Medical Research Council Unit at Hamnersmith Hospital. The radioactive 

half-life is 52 h and decay is by electron capture. The associated 279 keV gamma 

ray is detected by the photoelectric effect in garrena spectrometers. The methods of 

measvrement have previously been described (Chamberlain et al. 1975). 

212 Another radioactive isotope of lead, Pb, with a radioactive half-liTe of only 

10.6 h has also been used to study deposition in the lung and uptake to blood 

210 

(Booker et al. 1969, Hursh and Mercer, 1970). The long-lived isotope Pb, halflife 22 years, has been used for animal studies. 

203 The relatively short half-life of Pb, and the mdde of its decay by electron 

capture, limit the radiological dose to the subject. Also equipment and subjects 

are free of radioactivity and available for further experiments in a comparatively 

short period, since the radioactive decay reduces the activity by a factor of 100 in 

14 days. This also means that the uptake and excretion of any one dose can only be 

followed for a similar period. In extrapolating the results of experiments to the 

case of chronic exposure, certain assumptions have to be made, which can be verified 

only by reference to long term studies by other methods, reviewed in Section 10 of 

this report. 

To obtain labelled motor exhaust, tetra ethyl lead (TEL) was synthesised from 

the radioactive PbCl2 by a Grignard reaction and added to lead-free petrol together 

with an appropriate amount of ethylene dibromide scavenger. The concentration of 

TEL in the petrol was equivalent to 0.5 g Pb/1. A single-cylinder, high compression, 

4-stroke Honda engine was coupled to a generator to provide a load. The engine was 

-50-
P.52 

wermed-up on ordinary leaded petrol and then switched to the labelled petrol, which 

was consuned in a few minutes. There was S% of CO in the exhaust gas, and this had 

to be reduced before it was inhaled. This was done in two different ways, which also 

gave different lead concentrations and particle size. 

(a) Wind-tunnel aerosols 

The exhaust was passed into a wind-tunnel operated in the single-pass mode 

with an airflow of 2.5 m/s (Fig. 5.1). The 00 in the tunnel was less than 

1000 ppm, which was low enough for inhalations lasting a few minutes. The lead 

concentration was usually about 40 ng it" , and in a typical experiment abcwt 0.4 

203 Mg of lead, with 100 nanocuries (nCi) of Pb activity, was deposited in the 

lung. 

The particle size of the wind-tunnel aerosol was measured by similar methods 

to those used for the motorway aerosol. The diffusion battery was used to 

measure the diffusion mean equivalent diameter (CMED). The fractional penetra203 

tion through the battery was obtained from the ratio of Pb activity in the 

upstream and downstream air, whereas in the environment the stable Pb was 

measured. Andersen impactors were also used, but, in the wind-tunnel, all the 

particles penetrated to the filter, implying none greater than 0.3 um diameter. 

The aerosols were also sampled by thermal precipitators for electron microscopy 

(Fig. 5.2); and the volune mean diameter (VMD) deduced from the micrographs 

agreed well with the CMED from the diffusion battery (Table 5.1). 

When the exhaust was injected into the tunnel immediately downstream of the 

impeller fan, an aerosol with CMED of 0.04 um was obtained, as in the earlier 

work of Chamberlain et al. (1975). Smaller particles, with CMED equal to 

0.02 Mm were obtained by more rapid initial dilution. The jet from a centrifugal blower (wind speed 40 m s" ) was mixed with the exhaust and the mixture 

passed down a tube 10 an diameter x 120 cm long into the tunnel operating as 

before. The aerosol formed was slightly smaller than any found in the field. 

A larger size (CMED = 0.09 Mm) was obtained by introducing a 20 1 delay vessel 

between the exhaust pipe and the wind-tunnel (Fig. 5.1). Between them, the 

0.02, 0.04 and 0.09 Hn aerosols covered the "nucleus mode" of particle size. 

Subjects inhaled by mouth through a non-return valve, exhaling via a glass 

fibre filter to a balloon (Fig. 5.1). The system was as used in the field 

except that the balloons replaced the dry gas meters used for volume measurement 

in the field. These gas meters were calibrated against the standard wet gas 

meter which was used in all laboratory work. In all cases the breathing was 

recorded by pressure transducer and chart recorder. 

203 The inhaled concentration of Pb was measured by concurrent sampling from 

the wind-tunnel and the equipment lines. The volumes of the parts of the 

equipment were minimised and corrections were made for double-swept volumes when 

203 calculating retention. Deposition of Pb in the rig was measured by gamma 

counting and appropriate corrections made. The losses were mainly by diffusion 

and were most important for the smallest particle sizes. 

-51-
P.53 

For proper operation of the non-return valves, it WB S found necessary to 

operate the tunnel at a slight negative pressure (about 1 cm HjO), which wee 

done by use of a- extract fan at its outlet. Thla also prevented externnl 

203 contamination of the subject by Pb leaking from the tunnel 

(b) Box aerosols 

The 600 1 box previously used for storing the aerosol (Chamberlain et al. 

1975) was also used in the current work, both with exhaust aerosol and with 

aerosols made by burning TEL in propane. By the addition or elimination of 

nitrogen from the flame, lead nitrate and oxide aerosols were obtained. Concentrations of CO and CO, in exhaust aerosol were reduced by reaction with an 

oxidative catalyst (Hopcalite) and moist NaOH pellets on the floor of the box. 

CO was reduced to 1000 ppm in about one hour. Meanwhile the particles 

coagulated and formed chain aggregates (Wells et al. 1977, Fig. id). In some 

experiments the aerosol was exposed to sunlight for several hours before 

inhalations took place. In sane others by varying the running conditions of 

the engine (riyh mivt^re. no load) a carbonaceous aerosol was produced 

(Wells et al. 1977, Fig. la). 

203E 

The confinement of the aerosols in the box enabled higher concentrations of 

-3 

Pb to be obtained than in the wind-tunnel. Typically, 1 to 2 MCi were 

deposited in the lung in each experiment. This was the minimum activity 

required to enable the concentrations in blood and excreta to be followed for 

14 days. The concentration of stable lead was higher in the box than in the 

wind-tunnel, and varied considerably between experiments. The minimum level 

was set by the need to use at least 50 mg Pb carrier in the synthesis of the 

labelled TEL. The concentration of Pb in the box varied from 4000 to 200 Mg m 

but each inhalation lasted a few minutes only. In the whole serie s of windtunnel and box experiments, the amount of Pb deposited in the lung varied by 

three orders of magni tude, from 0.3 to 450 Mg, but no associated effects on rate 

of clearance or uptake to blood were found (Section 6.10). Even at the upper 

limit, the amount of lead entering the blood from the lung in one experiment was 

considerably less than the amount (typically about 1 mg) normally circulating. 

The particle sizes of the box aerosol were measured by use of the Andersen 

impactor (Table 5.2). The MUED was in the range 0.35 to 0.70 um for the 

exhaust aerosols and 0.40 to 0.80 um for the oxide and nitrate aerosols. 

The methods of inhaling from the box and measuring the deposition in the 

lung were as described by Wells et al. (1977). 

5.3 Deposition of labelled aerosols in the lung 

5.3.1 Wind-tunnel aerosols 

Table 5.3 shows the measurements of lung deposition of the wind-tunnel 

aerosol. Eight subjects took part in these experiments, but i t was not possible 

to perform sufficient replicate experiments to distinguish between-subject variation from the other variables. Experiments were done with three particle 

-52 -
P.54 

sizes (0.02, 0.04 and 0.09 M» CMED). Breathing parameters were tidal volume 

(litres/breath) and length of the respiratory cycle (seconds/breath). These 

were varied considerably in the experiments with 0.02 Mm particles, but less so 

for the other particle sizes. 

As in previous experiments (Chamberlain et al. 1975), the percentage of the 

inhaled aerosol which was deposited in the lung was measured by two methods 

203 

(a) comparing the activity of Pb on an exhalation filter with the activity 

inhaled, as deduced from the volume inhaled and the activity per unit volume 

of air, 

203 

(b) assessing the Pb deposited in the lung by external gamma ray spectrometry 

and comparing this with the activity inhaled. 

As shown in Table 5.3, there was good agreement between the two methods of 

estimating deposition in the lung. The percentage deposition corrected for 

dead volvme as shown in Table 5.3, is plotted against the length of the breathing 

cycle in Fig. 5.3. Percentage deposition increased with decreasing particle 

size and with increased length of respiratory cycle, as expected for sub-micron 

particles deposited in the lung mainly by Brownian diffusion. 

For the 'Standard Man' respiratory cycle of 4 s (15 breaths/min). deposition 

varied from 249? for the 0.09 um aerosol to 685? for the 0.02 Mm aerosol. In the motorway inhalation experiments (Table 4.1), the respiratory cycle averaged 5.3 s, and the 

lead aerosol had a DMED of about 0.035 \im (Table 3.7). Interpolating between the 0.02 

and 0.04 um curves in Fig. 5.3, about 56$ deposition in the lung would be expected, 

compared with the average of 61"? found in the field work (Table 4.1). 

5.3.2 Box aerosols 

Aerosols of 'clean' exhaust, carbonaceous exhaust, 'clean' exhaust exposed 

to sunlight, lead nitrate and lead oxide were inhaled with the main object of 

testing effect of chemical state on lung clearance. Subjects took long deep 

breaths (mean and S.D. of respiratory cycle 9.3 i 3.1 s, tidal volune 1.8 ± 0.5 1) 

to maximise deposition. The percentage deposition is shown in Table 5.4 and 

Fig. 5.4. The exhaust aerosols were deposited more effectively than the oxide 

or nitrate aerosols although the particle sizes of the latter were greater. 

The results were normalised to a tidal volume (V_) of 1 1 by applying 

factors derived by Wells et al. (1977). In Fig. 5.5 the curves showing the mean 

relation between percentage deposition and length of the respiratory cycle, with 

and without the normalising factor, are compared with similarly treated data from 

the earlier Inhalation series of 1974 (Chamberlain et al. 1975) and 1975 (Wells 

et al. 1977). The 1975 results, for unknown reasons, give lower deposition for 

short breathing cycles and a less steep rise with increased length of cycle. 

The same equipment and techniques were used for both series and the aerosol 

characteristics were similar as determined by both electron microscopy and 

Andersen impaction sampling (Table 5.2). 

-53-
The field inhalation experiments in the 'general urban' and 'car park' 

areas gave a mean stable lead deposition of 46% for a mean respiratory cycle of 

5.5 s. This is a higher deposition than was found In any of the box aerosol 

series, but as previously pointed out, the ambient aerosol had a wider particle 

size spectrum than the box aerosol. 

5.3.3 Comparison with other published work 

The variation of percentage deposition in the lung with particle size 

according to several investigators is shown in Fig. 5.6. From the present work, 

the results for 0.02, 0.04 and 0.09 Mm particles were taken from Fig. 5.3 with 

4 6 breathing cycle (15 breaths/min) which is the standard ICRP figure for resting adult males. The mean of the results of the three series in Fig. 5.5 has 

been used to derive a point for 0.5 Mm kMED. The computed curve of James (1978) 

203 

agrees well with the Pb results. Earlier calculations by the Task Group on 

Lung Dynamics (1966), not shown in Fig. 5.6, gave higher percentage retention 

for very small particles. The experimental results of Heyder et al. (1975) and 

Mitchell (1977), and the calculated curve of Yu and Taulbee (1977), all referring 

to a tidal volume of 1 1, show considerable variation in percentage deposition 

for particles of about 0.5 um VMED. This is also the size for which the Pb 

results are most variable (Fig. 5.5). 

5.3.4 Variation between individuals 

In the analysis of results, possible systematic differences in efficiency 

of deposition between individual subjects have not been taken into account. In 

the analysis of variance of the deposition of stable lead (Table 4.1), betweensubject variance fell just short of significance at the 556 level. 

For two subjects who took part in several series of experiments, the relative percentage deposition is summarised in Table 5.5. The results have not 

been normalised for tidal volume or length of respiratory cycle, but these were 

comparable in most cases. 

-54-
P.56 

- " * •>- 1— 'TT-Tlt 

TABLE 5.1 

Particle size of wind-tunnel Pb exhaust aerosols 

Series 

1975 

1977 

II 

1977 

•i 

II 

. Method 

Direct injection 

with load 

Pre-dilution 

no load 

it II 

Pre-delay 

with load 

it ti 

ii it 

Particle siz e (Mm) 

From electron 

micrographs 

VMD 

Mm 

0.035 

0.018 

0.022 

0.085 

0.112 

0.092 

Og 

1.5 

1.5 

1.5 

1.6 

1.5 

1.4 

Diffusion battery 

IMED 

Mm 

0.039 

) 

) 0.019 

! 

0.080 

0.090 

-55 -
TABLE S.2 

Aggregated aero«ols 

Andersen Impactor Data 

i l l 203 Pb-labelled exhaust aerosols (197S-IP77) 

Stage 

0 

1 

2 

3 

4 

S 

6 

7 

8 (filter ) 

Age at 

sampling 

<»in) 

SO* 

cut-off diam. 

U.S 

9.5 

5.7 

4.2 

2.2 

1.0 

O.S 

0.3 

Percentage deposited per atage 

Clean exhaust 

U A exposed 

7/7/76 

0.1 

0.0 

0.1 

0.1 

0.1 

46.3 

45.4 

S.B 

2.1 

350 

Clean 

exhaust 

23/3/77 

0.1 

0.2 

0.2 

0.4 

1.3 

4.2 

25.3 

62.5 

5.7 

112 

Carbonaceous 

exhaust 

20/4/77 

0.2 

0.1 

0.1 

0.3 

0.8 

0.8 

24.1 

64.3 

4.2 

110 

Carbonaceoua 

exhaust 

IB/5/77 

0.1 

0.2 

0.3 

0.3 

0.6 

4.8 

20.5 

59.3 

13.7 

110 

203, 

(2) Pb-labelled lead compounds (1976-1977) 

' Stage 

0 

1 

2 

3 

4 

5 

6 

7 

8 (filter ) 

Age at 

sampling 

(atin) 

Nitrate 

18/8/76 

0.1 

0.2 

0.1 

0.2 

O.S 

36.1 

38.9 

8.6 

15.1 

76 

Percentage deposited pe 

Nitrate 

7/9/76 

( i ) 

0.4 

0.4 

0.3 

0.3 

0.3 

0.6 

4.3 

35.5 

58.0 

30 

(ii ) 

0.2 

0.2 

0.2 

0.3 

0.5 

56.3 

39.4 

2.5 

0.5 

250 

Oxide 

10/11/76. 

0.1 

0.2 

0.2 

0.2 

0.3 

10.7 

43.1 

39.2 

6.3 

72 

r stage 

Oxide 

25/11/76 

0.2 

O.I 

0.2 

0.2 

0.3 

5.4 

37.5 

44.2 

12.0 

66 

Oxide 

30/11/76 

0.1 

0.2 

0.5 

0.2 

0.7 

10.4 

59.6 

22.9 

5.6 

94 

(3) 203, 

Pb-labelled exhaust aerosols (1975) (Wells et al. 1977) 

Stage 

0 

1 

2 

3 

4 

5 

6 

7 

8 (filter ) 

'Age at sampling (atin) 

Percentage deposited per stage 

2/I0/7S 

0.04 

0.04 

0.04 

0.1 

0.3 

10.1 

63.1 

24.6 

1.7 

164 

3/10/75 

0.07 

0.04 

O.OS 

0.1 

0.3 

5.4 

82.8 

10.8 

0.5 

• •3 

-56-
P.58 

TABLE 5.3 

Deposition in lung of wind-tunnel aerosols 

Particle 

diameter 

urn (CMED) 

0.02 

0.04 

0.09 

Subject 

ON 

DN 

MJH 

MJH 

ACKACK 

ACC 

ACC 

ACC 

AOC 

ACW 

ACW 

MJH 

MJH 

ACC 

DN 

RFH 

DHFA 

KEB 

ACC 

MJH 

MJH 

DHFA 

KFB 

RFH 

PL 

ACW 

PL 

MJH 

Resp. 

cycle 

s 

3.7 

11.3 

6.6 

11.7 

4.2 

20.9 

3.6 

7;6 

3.6 

2.4 

5.5 

0.8 

8.4 

7.5 

3.8 

4.1 

7.2 

6.6 

6.6 

4.2 

9.0 

5.7 

6.1 

7.0 

6.3 

5.2 

7.4 

4.5 

5.6 

Tidal 

volume 

1 

0.63 

1.25 

1.17 

1.45 

1.43 

2.11 

0.31 

0.39 

0.36 

0.34 

1.17 

0.43 

2.07 

1.25 

0.76 

0.84 

1.15 

1.31 

1.07 

-

-

0.79 

0.85 

0.97 

1.10 

0.72 

0.88 

0.70 

0.78 

% Deposition 

Filter* 

66.2 

80.0 

61.2 

84.6 

82.3 

91.6 

65.5 

72.7 

46.5 

45.5 

79.9 

-

63.0 

51.7 

32.9 

44.0 

58.5^' 

57,0 

56.1 

45.1 

60.0 

25.2 

35.6 

35.1 

Whole body 

counter 

67.0 

80.5 

79.7 

85.5 

64.1 

91.7 

-

80.7 

52.3 

52.3 

76.0 

38.4 

56.9 

46.9 

37.4 

\ 44.6 

'?•' 56.3-

52.9 

57.5 

44.6 

58.8 

20.8 

35.5 | 

34.9 \ 

41.4 |>?-*-" 45.6 / 

37.8 | 39.9 / 

24.8 27.8' 

34.4 34.4 

25.3 21.9 

Mean % 

deposition** 

70.4 

83.0 

83.4 

.. 87.6 

85.8 

92.9 

70.4 

86.2 

51.1 

53.0 

80.7 

39.6 

60.8 

50.2 

36.1 

45.6 

58.9 

56.0 

58.4 

46.6 

61.2 

23.3 

36.3 

35.7 

44.4 

39.9 

26.7 

35.3 

24.0 

* Comparison of Pb in inhaled and exhaled air. 

Corrected for the effect of dead voliane in apparatus. 

-57-
TABLE 5.4 

203, Deposition in lung of aggregated exhaust and other Pb-labelled aerosols 

Date 

7/7/76 

18/8/76 

7/9/76 

10/11/76 

25/11/76 

30/11/76 

23/3/77 

20/4/77 

i 18/5/77 

1 

i 

Type of aerosol 

Clean exhaust 

exposed t o 

sunlight 

Lead nitrat e 

Lead nitrat e 

Lead oxide 

Lead oxide 

Lead oxide 

Clean exhaust 

Carbonaceous 

exhaust 

Carbonaceous 

exhaust 

Subject 

MJH 

DHFA 

KFB 

MJH 

DHFA 

RFH 

ACC 

MJH 

RFH 

ADC 

DHFA 

DN 

KFB 

MJH 

MJH 

ACC 

DN 

RFH 

% deposition in lung 

Filte r 

48 

55 

34 

26 

26 

45 

62 

31 

41 

30 

14 

42 ' 

31 

39 

36 

36 

1 

! 40 

;

 4 3 

Whole 

Body 

Counter 

51 

44 

28 

26 

14 

39 

53 

28 

41 

26 

19 

43 

30 

33 

36 

38 

41 

41 

Mean 

49. 5 

49. 5 

31. 0 

;26 

20 

V§2 

57. 5 

29.5 

141 

28 

16.5 

42. 5 

30.5 

36 

36 

36 

41. 5 

42 

Tidal 

volume 

1 

2.0 3 

1.90 

1.69 

1.89 

1.76 

1.85 

1.73 

1.76 

1.73 

1.61 

1.73 

1.73 

1.69 

2.28 

1.80 

1.74 

1.76 

1.76 

Breathing 

cycl e 

s 

9 . 3 

7.4 

5.8 

9 . 3 

7.7 

8 . 3 

10.0 

14.6 

14.5 

7 . 0 

5 . 9 

17.6 

12.6 

9 . 5 

8 . 5 

6.6 

7.4 

5.7 

TABLE 5.5 

Variation of deposition in lung between two subjects 

Type of aerosol 

Laboratory - wind-tunnel 

Laboratory - aggregated 

Field - open road 

Field - general urban 

Field - multi-store y car park 

Deposition rati o 

PL/MJH 

1.46 

1.20 

1.16 

1.50 

1.29 

Nunber of 

observations 

1 

7 

4 

1 

3 

i 

Mean of individual observations 1.25 • 0.1 3 S.D. 

-58-
c 

c 

3 

+m 

•o 

«- c 

lri*J .? E 

"-e SS "5 O) •) *" 2 cc • • ? si 

u 

3 

- 5 9 
•"'.:';.•••• • \ ^ * . * * 

%V -Ly % 

, .. f .., , . •.?••• • ••*•..'• if 

" •»••• • ' •* ; r - • • . . 

: . . * •'• • - ' » ' • ' • »-.-.• ' "••;• • •••«"' . 

s

 ":-:•• . •• • .^^';-^ ! • * • • '•••:•.- • 

• 

" • ' *v . ..-,, . ,•// ? 

v*-. :- * - ••" - •*•'•'• * •••' * 

• •• • .•',.'» • a :.:••• - • 

I- » - .. .- » • • • » 

•••'"•«•-.• • • • • " 

*. •': • » ' ** . ' a \ * • * 

i. • 

0 1 .•:••;.- •

 f • - - -.*• V- *•."••*..• • v 

o Sis'.--**/-:;..'/;•• v*>••:*/. '• U-V^-V- ^ 

.''•-•• • ..••* • a , » . 

' • . - •• " . •• • • " .«•=•"*• ' • '• • .* • * • 

• v . .'•* -v r - .••••. • v .•--.. ;•• • 

.»..- . i ••• • •• .*••_• • • .-•-... -

• • * i-- *.. : , •* .* . • y-v" "-

, I — J v • 

• i . 

» / " •WV 

(a) (b) <c) 

AERE - R 9198 Fig. 5.2 

Wind tunnel exhaust aerosols used in inhalation experiments (a) 0.02 pm DMED, (b) 0.04 pm 

DMED. (c) 0.09 pm DMED 
' "-"•" TV'" ' *V2 4 6 8 10 12 

Breathing cycle (seconds) 

AERE. R 9198. FIG. 5.3. DEPOSITION IN LUNG OF WIND TUNNEL AEROSOLS. 

-61 -
- •*T"T T "T'l'ff *• •ITTI*" " 

, x Exposed to sunt.ght 

E^ou^* ^ [* ^onaceous * 

f A Lead oxide PbO 

l a Lead nitrate Pb (N03 ) 2 

6 8 10 

wreathing cycle (seconds) Bi 

AERE . R9198 FIG SA. DEPOSITION IN LUNG OF *0 3Pb LABELLED 

AGGREGATED AEROSOLS 1976-1977 PERCENTAGE DEPOSITION v. 

BREATHING CYCLE 

-62-
c 60 

o 

l/l 

o 

Q. 

ft 

•o 

| 40 

"c 

•> 

o 

a. 

0) 

20 

P.64 

ll 

0? 

^ V / .,o*°* ,o\* 

A * ° 

*** >rfS**!v*1 

1 1 1 1 1 

6 6 10 12 U 

Breathing cycle (seconds) 

16 

AER E R9198. FIG. 5.5. DEPOSITION IN LUNG OF AGGREGATED 

AEROSOLS. COMPARISON OF MEAN DEPOSITION CURVES. 

-63 -
A> 

f 

c 

3 

C 

O 

4/1 

o 

Q. 

o 

CL 

no 

70 

60 

50 

40 

30 

20 

10 

— 

— 

— 

1 

\ \ 

V 

• \ * 

1 

' © 20'

3

pb 

© Heyder 

- ! 3 1 

data I VTa1000crrT} 

1975 I VT»1000cm3) 

©MitchelM977 (VT = 1000 cm3) 

© James 

©Jame s 

\ © Yu 

\\X.© 

©v'\©\ 

> 

1 1 

1978 (VT=1000cm3) Calculated 

1978 (VT =500cm 3) Calculated 

1977 (VjslOOOcm3) Calculated 

Breathing cycle 4 seconds TM 

\ ^ ^ 0^ 

:

^--~^ > " \ -

..j^>*. c£).^ 

^^^"" ^ -

i i 

0 01 DMED 0 1 fim MMED 10 

A.E.R.E. R9198. FIG.5.6. A COMPARISON OF PUBLISHED DATA ON THE DEPOSITION IN THE 

LUNG OF SUBMICRON PARTICLES. 

-r 
/ 

r<, 

7V-, ' •'"/ 

6. Clearance of labelled aerosols from the lung 

6.1 Object of experiments 

Previous work (Booker et al. 1969, Chamberlain et al. 1975) had shown that radioactive lead deposited as particulates in the pulmonary region of the lung is removed 

almost completely in a few days. Most of the lead passes through the lung membranes 

and is redistributed in the circulation. Only amall amounts are brought up by 

ciliary action and swallowed or transferred to lymph nodes. Much of the lead in 

fresh exhaust is present as halides and is quite soluble in water. There remained 

the question, whether lung clearance would be different if lead aerosols of other 

chemical forms were inhaled. 

6.2 Methods of measuring rate of clearance 

203 Chamberlain et al. (1975) gave a method of estimating the proportion of Pb 

deposited in the lung which was still there at various times after inhalation. A 

pair of colllmated sodium iodide crystals, one above and the other below the chest of 

203 

a supine subject, responded to the gamma rays from Pb in the lungs and surrounding t

yc\\ 

tissues. The contribution from Pb in the chest but not in the lung was estimated 

from the response of similarly placed counters in separate experiments in which Pb 

was injected intravenously. After both inhalation and injection, measurements were 

203 also made of systemic Pb in the legs and also venous blood samples were analysed. 

203 Thus the contribution to the response of the chest counters to systemic Pb which 

203 had entered the blood stream from the lung could be assessed. The Pb remaining 

in the lung was then estimated and related to the time since inhalation. The present 

experiments differed from those previously reported in that 

(a) more subjects were used 

(b) in some experiments, Inhalations were of less duration and measurements of 

lung burden began very soon afterwards 

(c) subjects were repositioned in the counting equipment several times to reduce 

errors 

(d) a variety of lead aerosols was used. 

6.3 Results of lung clearance experiments 

The wind-tunnel and aggregated box aerosols described in Section 5.2 were used 

for these measirements. The inhalations usually lasted for 3-6 minutes and the first 

chest measurement was made at 5-8 minutes from the mid-time of the inhalation. 

Measurements were continued to at least 120 hrs and with the carbonaceous aerosols to 

260 hrs after inhalation. The results are shown in Figures 6.1 to 6.5 (in a log x log 

presentation). In each experiment there is excellent agreement between subjects. 

The mean clearance curves for each type of aerosol are compared in Fig. 6.6. The 

early clearance characteristics are very similar but there is some separation by type 

or aerosol at later times. The soluble compound Pb(NO,), and the very finely divided 

wind-tunnel aerosols were reduced to \% residue in the lung most rapidly (60-60 h) 

whereas the carbonaceous exhaust aerosol was only reduced to 10*1 at 100 h. The 

-65-
results with other aerosols - clean exhaust, exhaust exposed to sunlight, and PbO - lie 

close together between these limits. The clearance of the various exhaust aerosols is 

plotted in Tl*. 6.7 on log x linear axes and Compared with data previously published 

(Chamberlain et al. 1975). The curves are not simple single or dcuble exponential 

functions, but can be fitted by a aeries of exponential terms, the goodness of fit 

improving with the number of terms. A fair fit can be obtained with four terms. The 

resulting half-lives and contributions are listed in Table 6.1. Two of the clearance 

curves (lead nitrate and wind-tunnel exhaust) are well represented by three terms, 

having no long half-life component. If the aggregated carbonaceous aerosol is omitted 

from Table 6.1, the pattern is very similar, approximately 22% cleared with T, = 0.8 h, 

34*? with T^ a 2.5 h, 13% with T^ = 9 h and \2% with T^ = 44 h. This reflects the basic 

similarity of the curves in Fig. 6.6. The curve for carbonaceous aerosol is clearly 

different, with longer half-lives for a substantial fraction of the deposit. 

The similarity in clearance of exhaust aerosols and oxide aerosols from the lung 

is surprising when compared with the in vitro solubilities of the same aerosols 

measured by a small scale continuous flow technique (Fig. 6.8). The oxide appears 

less soluble in vitro than would be expected frcm the rate at which it is taken up 

from the lung. This could be ascribed to more efficient flow and transfer in the lung. 

However the nitrate and exhaust aerosols are far more soluble in vitro than is apparent 

from the lung measurements. This is possibly because the mechanism for transferring 

lead from lung fluid to blood is a relatively slow process which determines the overall 

transfer rate. 

With the exception of the carbonaceous aerosol, the residual lead left in the lung 

was less than \% of that deposited at seven days and was still falling. With the 

203 carbonaceous aerosol, the radioactive half-life of Pb is not long enough to permit 

a similar determination, but at 10 days the residual level was probably less than 7% 

and still falling. Barry (1975) analysed tissues for lead post mortem and found no 

concentration of lead in lung tissue relative to other soft tissue. This suggests 

that almost all the lead aerosol is absorbed from the lung or cleared by other 

mechanisms. 

6.4 Transfer from lung to blood 

203r Several venous blood samples were taken after inhalations of Pb, and Fig. 6.9 

shows the entry of 203„ 

I 

Pb into blood from the lung. In this and other figures, error 

bars indicate - 1 SE. The form of the curves is very similar to those obtained previously in the 1973/4 series of experiments with Pb-labelled exhaust and also to 

those obtained with nPb attached to condensation nuclei in air (Booker et al. 1969). 

This again shows that the chemical form or the lead in sub-micron sized particles made 

littl e difference to the clearance from the lung and transfer to blood. The level of 

203„ 

Pb in blood reached a peak about 30 h after inhalation. At this time the amount in 

blood, calculated by multiplying the specific activity in the samples by the subject's 

blood mass, was about 60% of the Initial lung burden. As discussed below In Section 7, 

this does not mean that 40* is still in the lung, since a similar percentage is found 

in blood after saline injection. 

-66-

•»•> II )J. 1 'l.BJH-1'U.'ll'.U.-U.!'. -.JU.ULIH 
P.68 

6.5 Dosage of stable lead 

In the inhalation experiments, for a variety of reasons already discussed, the 

quantity of stable lead deposited in the lungs ranged from 0.3 to 450 pg. This 

compared with 5 pg Pb intravenously Injected, and from 5-40 pg Pb absorbed from the 

gut in ingestion experiments. For comparison, urban exposure at 1 Mg Pb/m and 50X 

retention would result in the deposition of 8 Mg Pb per day in the lung. The possibility that the dosage level of lead affected the results needs examination. Two 

aspects can be considered - lung clearance and peak level in blood. 

Lung clearance curves for box exhaust aerosol (mean and S.D. Pb deposited in 

lung 11 t 4 Mg), wind-tunnel exhaust aerosol (1.5 ± 1.3 Mg) and box lead oxide aerosol 

(164 i 70 pg) are shown in Fig. 6.10. This is not a strict comparison of like with 

like - the wind-tunnel particles were much smaller and the oxide particles were 

chemically different from and rather larger than the aggregated exhaust. However it 

is clear that no major difference in lung clearance was produced. 

Levels of lead in blood (at 48 hrs) are compared for individuals in Fig. 6.11 and 

in normalised form in Fig. 6.12. The fitted regression line shows a small positive 

slope but the relationship is not significant at the 10$ level. 

-67-
.f,r - 7 --• ,-.- ^jrnf- • 

P.69 

Lung clearance following ir. 

203 

of Pb-labelled aerosols 

Comparison of exponential coi :nts of the observed mean 

clearance curves for s. different aerosols 

Aerosol 

Class 

Exhaust 

n 

» 

it 

Compound 

ti 

Description 

Aggregated, 

clean 

Aggregated, 

clean, U.V. 

Wind-tunnel, 

clean 

Aggregated, 

carbonaceous* 

PbO 

Pb(N03)2 

Component half-live s and 

I 

Tm 

h 

0.6 

0.6 

1.2 

0.5 

0.5 

1.0 

% 

16 

23 

27 

29 

25 

26 

II 

h 

2.6 

2.7 

2.3 

4.5 

2.9 

2.2 

* 

36 

31 

39 

50 

32 

33 

percentage contributions 

III 

Tm 

h 

8.0 

9.1 

8.1 

24 

9.8 

% 

36 

36 

34 

6 

25 

IV 

h 

42 

52 

-

220 

38 

! 

10.0 • 41 

% 

10 

10 

-

15 

18 

-

* Data for R.F.H. omitted. 

-68-
100 

A. 

I 

c 

3 

Ot 

c 

o 

E 

Ol 

O 

c 

u 

«_ 

OL 

10r1 

> 

"~ •+ ACC 

x MJH (1) 

0 MJH 12) 

A DN (1) 

0 DN (2) 

O DHFA 

« MEANS 

I 

• I 

-

• 

1 i 

O

 A 

- \ 

\

e 

\ 

. V, 

•l-ve 

01 1 10 100 

Hours elapsed 

A E.R.E R9198 FIG 6.1. PERCENTAGE OF DEPOSITED

 203Pb REMAINING IN LUNG. WIND TUNNEL_ 

EXHAUST AEROSOLS (0i02/im| 

IS 
I 

? 

Ol 

c 

3 

Ol 

c 

c 

o 

E 

«* 

Ol 

o 

c 

u 

«_ 

a. 

10 

1 

x MJH 

O OHFA 

• KFB 

Jr. I 

01 1 10 100 

Hours elapsed 

AERE . R9198. FIG 6.2. PERCENTAGE OF DEPOSITED

 203Pb REMAINING IN LUNG. U/V EXPOSED 

EXHAUST AEROSOL 7/7/76. 
100 

7 

*-eorK&—^ 

Ol 

c 

3 

Ol 

c 

c 

o 

E 

?* 10 

Ol 

o 

c 

Or 

u 

'"" -^^oS**;-. 

^^^tft*^. 

^r«k < 

x MJH 

• MJH 

+ ACC 

• RFH 

A DN 

Cl ean exhaust 

Carbonaceous 

ii 

n 

it 

aerosol 

exhaust 

N 

II 

II 

aerosol 

it 

II 

II 

I 

01 1 10 100 

Hours elapsed 

A ERE . R9198. FIG. 6.3A. PERCENTAGE OF DEPOSITED

 203Pb REMAINING IN LUNG. CLEAN AND 

CARBONACEOUS EXHAUST AEROSOLS. 
100 

I 

-J 

K> I 

Ol 

c 

3 

Ol 

c 

o 

E 

0> 

o» 

o 

c 

d> 

o 

i_ 

a> 

a. 

*<&« , 

0 MJH 20/4/7 7 

4 ACC 20/4/7 7 

• RFH 18/5/7 7 

A DN 18/5/7 7 

X 

10 100 1000 

Hours elapsed 

AE R.E.R9198 FIG 6 3B. PERCENTAGE OF ?03Pb REMAINING IN LUNG. CARBONACEOUS EXHAUST 

AEROSOLS AT TIMES>10 HOURS. 

i U 
100 

w 

I 

c 

Ol 

c 

O 

E 

Ol 

o 

c 

tl 

u 

tm 

a» 

a. 

10 

0 1 

x MJH 

• RFH 

O DHFA 

+ ACC 

Ir*05 ir 

10 100 

Hours elapsed 

AERE . R9198. FIG. 6 U. PERCENTAGE OF DEPOSITED

 203Pb REMAINING IN LUNG. LEAD NITRATE AEROSOL 

i 

•1 
*«•• # 

o 

cc 

UJ 

< 

UJ 

o 

X 

o 

o 

< 

UJ 

o 

z 

Z> 

o 

z 

z 

< 

.o 

? «*• 

• o 

Q. 

o o 

T. UJ 

«ft 

< 

u. o x x 

x o u. -• z u. 

O < E Z O 3f 

6unj u; 6uiuiDUjaj a6ojueojad 

-74-

o 

3 D. 

O UJ 

X o 

u. 

o 

UJ 

o 

< 

UJ 

o 

cc 

UJ 

0. 

IT) 

to 

d 

CO 

o> 

oc 

ixi 

a 

UJ 

< 
I 

Ol 

c 

3 

Ol 

'c 

5 

E 

Ol 

O 

«• o. 

A E 

0*1 10 10 

Hours elapsed 

RE. R9198. FIG 6.6. COMPARISON OF THE LUNG CLEARANCE OF VARIOUS 

LABELLED AEROSOLS. 

100 

203 Pb 
P.77 

100 

Ot 

c 

3 

Ol 

C 

O 

E 

ft 

ft 

Ot 

O 

c 

ft 

o 

ft 

a. 

T — r r T r —T i 1— 

1973-74 data single - subject 

———- 1976-77 data multi-subject 

10 20 80 100 120 

Hours elapsed 

140 160 180 

AE R.E. R9198. FIG. 67. CLEARANCE OF VARIOUS EXHAUST AEROSOLS 

FROM THE LUNG. 

-76-
P.78 

-"nr" 

lOOart: 

•o 

ft 

> 

"o 

(A 

l/l 

"*5 

c 

3 

ft 

O) 

o 

c ft o 

tm 

ft 

QL 

10 

1 

2 

3 

4 

5 

In vitro solubility curves, at a constant 

rate of 0 5 ml per minute :-

Exhaust aerosol 

Exhaust aerosol 

Lead nitrate aerosol 

Lead oxide aerosol 

Lead oxide aerosol 

__Mean lung clearance curve 

( oxide / nitrate / exhaust aerosols) 

i I 

10 20 30 40 50 

Minutes elapsed 

60 70 6 0 90 

A.E.R.E.R9198.FI0.68. COMPARISON OF IN VITRO SOLUBILITIES WITH 

LUNG CLEARANCE. 

-77 -
OB 

I 

100 

80 

60 

40 

o 

o 

2

 2 0 

x» 

Q. 

O 

oi 

o 

c 

ft 

u 

10 

8 

1 

PbCl2_J°. 

VinejnJSillon 

1 _L _L X X JL ± 

0-1 0 5 1 2 5 10 20 50 

Time after intake (h) 

A.E.R.E. R9198. FIG. 6.9. LEVELS OF

 2 03Pb IN BLOOD FOLLOWING INHALATION OF EXHAUST 

OXIDE OR NITRATE AEROSOLS. OR INJECTION OF PbCI?. 
100 •»•••**•*. &w 

I 

•4 (0 

Ol 

c 

3 

Ol 

c 

]c 

o 

E 

ft 

«_ 

JQ 

Q. 

tn 

o 

r>i 

"O 

ft 

vi 

o 

CX 

ft 

"O 

ft 

Ol 

"c 

ft 

u 

i . 

& 

10 

10 

•?• x* x ^x f l *x*» 

^ • x • 

v.-

^ * » X * 

x 

{ x* 

* * . 

* x# # 

X « 

XX 

« * • 

x Aggregatedlbox) exhaust aerosol (9) 11±4//g Pb deposited in lung 

• n n PbO n <3> 164170/ig Pb II n II 

* Mean curve for wind tunnel exhaust aerosol (a) 1 5*1 3//g Pb deposited in lung 

x 

X X 

x 

X * 

01 1 10 100 

Hours elapsed 

A.E.R.E.R9198. FIG. 6.10. LUNG CLEARANCE AT DIFFERENT LEVELS OF STABLE LEAD DEPOSITION 
01 

t_ 

3 

O 

JZ 

OD 

TJ 

O 

o 

Xi 

c 

Jm\ 

a. o 

o 

CM 

ft 

Ol 

O 

c 

ft 

u 

ft 

CL 

1 10 

Stable lead deposited in lung (/ig) 

A.E.R.E. R9198. FIG. 6.11. RELATIONSHIP BETWEEN STABLE LEAD DOSAGE AND PEAK LEVELS IN 

BLOOD FOR INDIVIDUAL SUBJECTS. 

1000 

00 
-18

-

TJ 

m 

> 

x 

r~ 

m 

< 

m 

c~ ai 

z 

a ro 

o 

o 

A.E.R.E. R919 8. FIG. 6.12. NORMAL — t/» 

m 

o 

**o 

m r~ 

> IO

H N tn 

X TJ OJ 

m -* 

* 

m rn 

z 

</» - i 

> 09 rE- LEAD DOSAGE A 

z 

o 

w» »» 

o O" <0 

7 

o OL dap 

o 

</• 

— <• 

& 5' 

— 

c 

3 

*te" (O 

q 

© _» 

o _^ 

o 

o _* 

o 

Normalised percentage of

 203

Pb in blood at 

48 hours (Individual subject means 55% ) 

o 

vn 

o» 

o 

o 

o 

o 

1 

-

— ------

1 

1 

X 

x> 

> >: 

x

 X

x x 

1 

X 

X 

X x x

x — 

w 

X 

K X 

X X 

* X 

X 

X 

X 

1 * I X 1 * X 1

 x 

I

 x 

X 

X 

-

1 II . 

Z8d 
P.83 

7. Injection Experiments 

7.1 Object of experiments 

There were three main objectives 

(a) to observe the pattern of distribution in plasma, red cells and excreta of 

lead which had entered the blood in a very short period of time, 

203 

(b) to calibrate the response of the chest counter to systemic Pb, as 

described in Section 6.2, 

(c) to measure urinary and endogenous fecal excretion. 

203 

For these purposes Pb was injected intravenously as PbCl. in sterile normal saline. 

7.2 Methods 

Solutions for injection were made up with pyrogen-free normal saline and were 

sterilised by autoclaving. Carrier lead was added at the rate of 5 pg/ml. The 

203 activity of Pb injected was in the range 1.0 - 1.8 MCi. This enabled the activity 

203 in blood, urine and feces to be followed for 14 days. The activity of Pb in the 

syringe was measured by counting at a sufficient distance from a sodiun iodide scintillation crystal for the counting efficiency to be accurately reproducible. At intervals 

after injection, 20 ml of venous blood was withdrawn from an arm, heparin was added and 

cells and plasma immediately separated by centrlfuging. For early samples (2 - IS minutes post injection), the blood was withdrawn from the non-injected arm. The total 

•ass of blood for each subject had previously been measured by an isotope dilution 

technique employing I-labelled human serum albumin. Thus the concentration of 

203 203 

Pb in venous blood samples was also expressed as the total Pb in blood, or as 

the percentage in blood of the original injected dose. 

203 

7.3 Pb in blood following injection 

7.3.1 Interchange with extra-cellular fluid 

203 Fig. 7.1 shows the percentage of an intravenous dose of Pb which was 

present in the blood of three subjects at times from 1 to 200 min after injection. 

The percentage of the lead in blood which was in plasma is also shown, and a 

20**i 

separate curve shows the percentage in plasma in an experiment in which Pb was 

203 added to blood in vitro. At the time of the first sample (1.5 min) the Pb in 

blood represented only 45% of the injected dose. The sample was taken from the 

other arm, but circulation of the blood is sufficiently rapid that mixing should 

have occurred. The percentage fell further to 34$ at 3 min. Results from 3 

subjects agreed well. It was impracticable to take samples from one subject 

sufficiently rapidly to follow the time scale completely. From 4 min onwards, 

the amount of Pb in blood then recovered slowly, reaching 59# of the injected 

dose at 200 min. Other investigators have found 50 to 60JJ of injected dose of 

212 203 210 

Pb, Pb and Pb in the blood of human subjects and animals after injection 

(for references see Chamberlain et al. 1975). The peak activity in blood after 

inhalation also represents a similar fraction of the Initial lung burden 

(Section 6.9 and Fig. 6.9). 

-82-
The fraction of blood lead which was in plasma showed a rapid fall after 

injection, 63% being attached to red cells at 1.5 min. In vitro, 55*6 was 

attached to red cells after 1 min. The unattached fraction in vivo was 19% at 

10 min and less than \% at 1000 min. 

203 

7.3.2 Levels of Pb in plasma 

203 Fig. 7.2 shows the percentage of Pb in blood which was in plasma at 

times from 1.5 min to 30 h after injection. Results obtained following inhalation and ingestion are also shown. After inhalation, lead enters the plasma 

from the lung for some hours, and this maintains a higher percentage than after 

injection. From 10 h onwards, less than 0.3% of the Pb was in plasma. This 

is a such lower percentage than usually reported for stable lead. Cavalieri 

et al. (1978) reported 2 to 3% of the stable lead in plasma. However they added 

K.EDTA anticoagulant to blood before centrifuging. When EDTA was added in vitro 

203 to blood from a subject who had received Pb, progressive detachment from red 

cells was observed. In the present work heparin anticoagulant was used, and 

blood was centrifuged within a very few minutes of sampling. Hursh et al.(1969), 

212-

using the isotope T"b found 0.5 to 1.5% in plasma when heparinised blood was 

centrifuged 15 min after collection. 

7.3.3 Transfer from blood to sites of storage 

It seems that two processes are operating, as previously proposed by 

Stover (1959) 

203 

(a) a rapid sharing of the soluble inorganic Pb between plasma and other 

extracellular fluid (E.C.F.), 

(b) a rather less rapid attachment to red cells, which further depletes the 

plasma, reverses the concentration gradient with E.C.F. and draws some 

"^Pb back into blood. 

As the ultimate level in plasma is very IOVN-, all the lead would return to blood 

if blood and E.C.F. were the only compartments receiving lead. 

In the ICRP standard 70 kg man the volumes of E.C.F. and plasma are:-

plasma 2.8 1 

easily accessible E.C.F. 9.8 1 

less accessible E.C.F. 5.6 1 

Thus the ratio of volume of plasma to other E.C.F. is in the range 3.5 - 5.5 

depending on accessibility . 

203 At 3 min post-injection, 34% of the Pb remained in the blood and or this 

1/5 was in plasma. If the plasma is assumed to be in equilibri a with the E.C.F. 

203 

and the volune ratio is taken as 4.5 , then the distribution of the Pb between 

red cells, plasma, E.C.F. and other site s can be estimated. Table 7.1 shows 

possible distributions at 3 min and at 24 h after injection. 

This suggests that l/3 of the injected lead passes to other site s extremely 

-83 -
P.85 

quickly and ill et /.is fr^rcion continues to rise more slowly with time. There 

Is no cert •) ".•.it;/ .fex lY.i. storage locations at 3 min and 24 h are the same. By 

reference to ra^za jxper .stents, the most important storage site from a few hours 

210 onwards is probably bone. Hackett and Sikov (1977) injected rats with Pb and 

sacrificed them serially in groups. In the group killed 90 min after injection, 

30% of the original dose was in the skeleton, and this increased only slowly to 

40% in the group killed at 11 days. 

7.3.4 203, Pb in blood from one day onwards 

203„ The peak concentration of Pb in blood was reached about 10 hours after 

injection, at which time an average 59% of the dose was in blood. Similar peak 

percentages of the retained dose were found after inhalation (Table 7.2). This 

is further evidence that little of the lung burden was stored in lymph nodes or 

removed by ciliary action and swallowed. There was some difference between 

subjects (Table 7.3) but this may have been caused by errors in estimation of 

blood mass. If Instead of the result 5.7 kg for HJH's blood mass obtained by 

this method, there is substituted a figure of 5.1 kg estimated from HJH's height 

and weight, the entry in Table 7.3 is reduced from 70% to 63%. 

203 The concentration of Pb in blood declined from 1 day after injection 

exponentially (Fig. 7.3), till 14 days, beyond which time radioactive decay made 

the measurement inaccurate. In Table 7.4 the biological half-lives in blood 

following injection, inhalation and ingestion are compared. The differences in 

half-life between modes of entry are of doubtful significance. Work with the 

204 stable isotope Pb by Rabinowitz and his colleagues at UCLA, reviewed in 

Section 10.3, shows that removal of lead from blood continues to follow an exponential law for as long as 100 days after exposure ceases (Fig. 10.2). The 

biological half-lives shown in Fig. 10.2 are 18, 24, 36 and 18 days for UCLA 

subjects A, B, D and E respectively. Thus the mean Pb half-life of 18 days 

from the injection experiments (Table 7.4), though measured over a period of only 

204 14 days, agrees with that of Pb in two of the UCLA subjects. 

-84-
P.86 

H"TT^- i—TTI^HW TM 

TABLE 7.1 

203 Possible distribution of Pb after Intravenous saline injection 

Location 

Red blood cells 

Plasma 

E.C.F. 

Other locations (by difference) 

203 Percentage of injected Pb 

at 3 min 

28 

7 

32 

33 

at 24 hr 

55 

].' 

44 

Table 7.2 

203 Mean percentage of absorbed Pb appearing in blood at the 

peak for various groups of experiments 

Mode of Intake 

Inhalation, aggregated aerosol, 1974 

" " " , 1976-7 

Inhalation, wind-tunnel, 1975 

" , 1977 

Saline injection, 1974 

" " , 1977 

Ingestion, fasting, 1977 

Ingestion, with food, 1977 

203 

Peak Pb in blood 

(% of uptake) 

50.6 

56.0 

50.6 

55.4 

58.0 

58.9 

53.0 

50.1 

S.D. 

5.8 

8.5 

8.7 

5.6 

6.8 

5.0 

9.3 

12.2 

S.E. 

1.7 

3.5 

3.6 

2.3 

3.2 

1.8 

2.7 

3.5 

-85 -
P.87 

TABLE 7.3 

203. Peak levels of Pb in blood following intravenous inlection. 

Comparison of subjects with more than one administration 

Subject 

ACC 

DN 

MJH 

203 

Peak Pb in blood (% of uptake 

1977 

55.3 

53.6 

57.1 

57.9 

70.0 

1974 

55.0 

51.5 

69.0 

TABLE 7.4 

203, Biological half-lives of Pb in blood following intravenous 

saline injection compared with other modes of intake 

(Individual values for saline injection experiments) 

Subject 

AOC 

DN 

MJH 

ACW 

PL 

KFB 

ANBS 

Mean 

, 

Observed half-life in blood (T. 

Saline 

1974 

-

22.0 

14.9 

-

-

13.6 

-

18.3 

injection 

1977 

15.3 

15.7 

20.9 

23.2 

17.4 

21.6 

22.8 

13.9 

i 1 

1 3.6 S.D. . 

1.1 S.E. 

All 

inhalations 

13.6 (3) 

20.6 (2) 

16.1 (5) 

-

-

16.9 (1) 

-

16.4 1 2.2 

0.7 

in days) 

All 

ingestions 

12.9 (2) 

22.3 (1) 

14.0 (2) 

-

-

-

-

15.4 i 6.0 

3.6 

(Figures in brackets indicate number of experiments) 

-86-
~i i 

E 

_2 

o 

> 

•o 

o 

o 

Jfi 

O 

JC 

* 

.o 

Q. 

o 

JM 

1 

u 

« 

CT 

O 

c 

«l 

«J 

« 

CL 

40 

- 3 0 

a E 

«/i 

a 

a. 

c 

o 

<M 

•o 

o 

o 

20 o 

Ol 

o 

c 

01 

u 

I -

«l 

OL 10 

AE 

100 

Minutes elapsed 

RE R9198 FIG. 71. LEVELS OF 203pb IN BL000 FOLLOWING INTRAVENOUS INJECTIONS 

203, 

OF 

'PbCt2 IN SALINE 
100 

a , 

f 

o 

E 

a 

o. 

JD 

a. 

CO o 

CM 

*o 

o 

o 

a* 

"c 

a 

o 

S. 

~T ' r 

Saline injection 

Inhalation,exhaust 

exhaust 

U/V exhaust 

PbO 

PbO 

Pb(N03 ) 2 

ionlfasting J PbCl2 

T 

+ 

X 

A 

A 

o 

o 

* 

ANBS 

MJH 

DHFA 

KFB 

MJH 

ACC 

OHFA 

MJH 

ACC 

DN 

10/10/77 

8/10/7 7 

7 / 7/7 6 

7/7/7 6 

7/7/7 6 

25/11 / 76 

25/11 / 76 

18/ 8 / 76 

13/10/ 76 

13/10/76 

0 01 01 1 10 

Hours elapsed 

A.E.R.E.R9198. FIG. 7.2. PERCENTAGE OF 203 P b - N BLOOD IN THE PLASMA 

100 

oo 

CO 
100 

o 

o 

A, 

70 

<D .•= I 

o 

SO 

T • r T

 r 

«^*(? 

• 

X 

O 

A 

o 

® 

MJH 

DN 

PL 

ANBS 

ACW 

ACC 

cr 

1 1 I 1 I I 1 I 

t.0 80 120 160 200 240 280 320 

Hours elapsed 

AE R.ER9198 FI0.73.

 203Pb IN BL000 NORMALISED TO 100 AT 60h AFTER INTRAVENOUS SALINE INJECTION OF ?03PbC«2 ; 
P.91 

203 

8. Excretion of Pb 

8.1 Object of measurements 

203 The objectives of measuring Pb in urine and feces were 

(a) to compare loss by excretion with the decline in the whole-body count of 

203 the subject after he had received Pb by inhalation or injection, 

(b) to determine the rate of endogenous fecal excretion, 

(c) to examine whether excretion of the radioactive lead was at a similar rate 

to that reported elsewhere for stable lead, by comparing Pb in excreta 

with the levels in blood, 

(d) to obtain information about the metabolic processes of excretion. 

As with other aspects of the work with Pb, the conclusions only apply directly to 

short term processes in the first two weeks after the lead was inhaled or injected. 

6.2 Methods 

Complete collections of urine were made in polythene containers to which carrier 

lead and preservative had been added. In some experiments a series of short samples 

was collected for the first 46 hours. Thereafter daily 24-hour collections were 

analysed. As all collections of urine were over specified times, excretion was 

expressed per hour and not per litre. In earlier work, the question was examined 

203 whether urinary Pb was better expressed per hour,per litre or per g creatinine. 

A complete collection of urine, in 28 samples, was made for 14 days after a subject 

had received Pb by injection of labelled red cells. The mean rate of excretion 

of creatinine was 0.064 g/h with standard deviation 0.009 g/h. Thus the coefficient 

203 

of variation for creatinine excretion was 14%. The variation in • Pb in urine 

expressed per hr or per g creatinine was similar and both were less than the variation 

in Pb per litre of urine. It was concluded that there was no advantage in measuring creatinine if all urine collections covered known periods of time. 

20*"i 

The Pb in the urine was estimated by placing aliquots on a 15 cm diameter 

sodium iodine crystal to record the gamma emissions. Lead tended to sorb on precipi203 

tates in the urine and this altered the counting efficiency for Pb. Wien this was 

discovered, it was corrected post facto by analysing the form of the gamma spectrum. 

203 

Thereafter 10 ml cone. HCI was added per litre of urine to keep the Pb in solution. 

203 Complete collections of feces were made and the Pb content measured. As voiding 

of feces may be irregular, it was necessary to average over several days to obtain 

excretion rates. 

It is useful to relate urinary and endogenous fecal excretion to the level in 

blood, thus 

renal clearance (g/h) = Amount excreted in urine per hour 

•** Amount per g of blood 

For the excretion of substances which are present in plasma, the denominator is sometimes amount per g or per ml of plasma. Lead is mainly In red cells, but the rate of ax o v 

»v 

V 

-90-
P.92 

urinary excretion is possibly related more to lead in plasma than lead in whole blood. 

Often the plasma lead is not separately measured and renal clearance can then only be 

expressed per g of whole blood. 

8.3 Excretion in urine 

Fig. 8.1 shows the rate of urinary excretion in the first 36 hours after intake 

of "^Pb by inhalation, injection and ingestion. The results are expressed as percentage per hour of the uptake. For inhalation experiments uptake is equated to the 

203 initial lung burden. For ingestion, it is the Pb remaining in the body after 5 

days, not that present at the time the urine was excreted, which would have included 

203 unabsorbed Pb. Following injection, urinary excretion was initially at the rate 

of \% per hour, but declined rapidly as the fraction of Pb in plasma declined 

(Fig. 7.2). From 4 hours, the excretion rate declined only slowly. The excretion 

following inhalation also declined with time, but the initial rate was not so high as 

203 

following injection, as it took some hours for the transfer of Pb from lung to 

blood. The graphs for excretion after ingestion in Fig. 8.1 show a peak after 4 hours 

(ingestion while fasting) and 8 hours (ingestion with food). The delayed appearance 

of the peak is related to the time for absorption from the gut. In Fig. 8.2 the 

urinary excretion after inhalation of 5 different aerosols by one subject is shown, 

and also the excretion after 4 subjects inhaled PbO aerosol. 

In the upper part of Fig. 8.3 is shown the urinary excretion, as percentage of 

203 the initial body burden of Pb, over the period 1 to 14 days. The results for 

saline injection and inhalation are similar from 2 days onward, and show a decline with 

a half-life of 19 days. This is similar to the half-life in blood, indicating a 

constant renal clearance rate (Section 8.6). The mean percentage excretion per day 

203 

over the period 3-14 days of 6 subjects receiving Pb by injection is shown in 

Table 8.1. The urinary excretion was fairly consistent between subjects, the 

coefficient of variation being 8%. 

8.4 Endogenous fecal excretion 

In the lower part of Fig. 8.3, fecal excretion in the 14 days following injection 

and inhalation are compared. In the first 4 days, fecal excretion was higher after 

inhalation than injection. Excretion of aerosol brought up by mucociliary action and 

swallowed may have contributed to this excess, which however only amounts to a total of 

about 3% of the initial lung burden. 

The percentage endogenous fecal excretion of 6 subjects from 3 to 14 days after 

Injection is shown in Table 8.1. The ratio F AJ of endogenous fecal to urinary 

excretion had the mean value 0.49 with standard deviation 0.15. It appears from 

Fig. 8.3 that endogenous fecal excretion is established within a day or two at the 

latest, allowing for delay in voiding the feces. Chamberlain et al. (1975) reported 

F ^ = 0.7 following inhalation. The figure for the injection experiments is slightly 

lower, partly because there'was some small contribution of swallowed Pb in the 

inhalation experiments, but mainly because two subjects (ANBS and ACW), whose FA ) 

ratios were la*, were not Included in the earlier series. Data for those subjects who 

took part in all the series of experiments are compared in Table 8.2 and the mean values 

-91-
P.93 

of F /U for inhalation and injection are seen to be in closer agreement though the 

•inhalation value is still the larger of the two. 

Ratios F Al of 0.7 and 1.1 have been found in two series of measurements on 

* 210 baboons injected with Pb (Cohen, 1970; Strehlow, 1971). In rats injected with 

•^Pb, F A* was about unity (Morgan et al. 1977). Harrison et al. (1966) injected a 

47 fi*\ \W 223 

healthy man with Ca, Sr, Ba and Ra and measured excretion in urine and 

feces for 8 days after each injection. Ratios F ^ of 0.48 (Ca), 0.75 (Sr), 9.0 (Ba) 

and 36 (Ra) were found. 

8.5 Total excretion 

203„ The combined rate of urinary and fecal excretion of injected Pb was 1.24** per 

203 day (Table 8.1). If no other route of excretion is significant, the amount of Pb 

in the subject, together with his cumulative excretion, should equal initial dose. 

This was tested in 6 subjects after injection (two of them on two occasions) (Table 8.3). 

The results showed a very satisfactory balance, and it may be concluded that other 

routes of excretion, for example in sweat, are not important. 

203„ 

8.6 Excretion in relation to Pb in blood 

Table 8.4 shows the rates of renal clearance and endogenous fecal clearance over 

the period 3-14 days after injection experiments. The renal clearance rate is 

defined by 

203 

Renal clearance (g/h) =

 A ^rMS P^excreted in urine per hour 

Average Pb per g whole blood 

and similarly for the fecal clearance. The average renal clearance of 3.82 g/h compares with 4.5 g/h (4.3 ml/h) found in the earlier series of inhalation experiments 

(Chamberlain et al. 1975). Kehoe (I96ia) round an average blood lead (PbB) of 

28 ug/100 g and average urinary output (PbU) or 30 Mg/d in 10 normal adults, which 

gives a renal clearance rate of 4.5 g/h. Rabinowitz et al. (1976b) found average 

PbB = 19.4 Mg/100 g and PbU = 35.6 ug/d in 5 subjects, giving renal clearance of 

7.7 g/h. There is evidence from Kehoe1s (1961b, 1966) work with subjects given oral 

doses of lead that PbU increased more rapidly than PbB, so that renal clearance rates, 

when expressed relative to whole blood, increased with increasing PbB. There have 

been few measurements of endogenous fecal lead in humans, owing to the difficulty of 

distinguishing i t from unabsorbed dietary lead in feces. Rabinowitz e t al. (1976b) 

204 

gave oral doses of the stable lead isotope Pb to subjects daily for periods of 

204 

several months. From 10 days after cessation of dosing onwards, Pb appearing in 

feces was ascribed t o endogenous fecal excretion, and analysis of these data 

(Table 10.4 below) shows that the rate was equivalent t o 2.5 g/h, compared with 

1.82 g/h for the AERE subjects in Table 8.4. 

By dividing the estimated blood mass of the subjects by the total (F • U) rate 

of excretion, a clearance half-lif e in days is deduced in the last column of Table 8.4. 

This would be the half-lif e of Pb in blood i r all excretion were from that compartment and there were no transfer from blood to other site s of storage. In Table 8.5 

the blood half-lif e (T^) calculated in this way is compared with the half-lif e calculated 

-92 -
P.94 

s from the decline of Pb in blood (Fig. 7.3). On average T^ calculated from Ffi • U 

is 50% higher than that calculated from the venous blood results. Thus over the 

203 period 3-14 days there was a net loss of Pb from blood to other storage sites at a 

mean rate of 1.2% of blood lead (or 0.5% of whole body lead) per day. 

If instead of using the total clearance rates in Table 8.4, the blood mass is 

divided by fecal clearance, the average result is 3030 hours, or 126 days. This 

203 would be the mean life of Pb in blood if excretion took place by the fecal route 

only. One source of endogenous fecal excretion is the bile, and one possible source 

of lead in the bile is the destruction of dead red cells in the liver. The mean 

life of red cells is reported to be 120 days, so the rate of endogenous fecal excretion 

corresponds to this rate of destruction. However, other elements, such as the alkaline earths, *tfiich are not preferentially concentrated in the red cells, are also 

excreted via the feces (Harrison et al. 1966) and the scavenging of moribund red cells 

by the liver could hardly account for the endogenous fecal excretion of these elements. 

203 8.7 Relation of urinary excretion to Pb in plasma 

203 Table 8.6 shows measurements of Pb in collections of urine and in plasma 

following a saline injection. The blood was centrifuged within a minute or two of 

sampling. Fig. 8.6 shows the renal clearance expressed as 

203 

renal clearance 

Pb excreted in urine per minute 

203, Pb per ml of plasma 

Graphs are given for the ingestion experiment of Table 8.6, for the mean of 7 inhalation experiments and for a fasting ingestion experiment. The plasma renal clearance 

rate increased to a peak 1 hour after injection. After inhalation and ingestion the 

peak was later, owing to the delay in uptake. The reason for the peak is not known. 

Irrespective of mode of administration, the plasma renal clearance was about 30 ml/min 

from 12 hours onwards. Glomerular filtration rates of order 100 ml/min are lound for 

a number of substances, for example Na, K, Cl, creatinine and glucose (Best & Taylor, 

19C1). 

The mean urinary excretion at 3-14 days after injection was 0.83% of the injected 

dose per day (Table 8.1), equivalent to 5.8 * 10 per min. Over that period about 

47% of the injected Pb was in blood. The average blood mass was 5230 g, blood 

203 volune 5000 ml and plasma volume 2740 ml. The mean percentage of Pb in blood that 

was in plasma over the period 10 to 100 hours was 0.24% (Fig. 7.2). Hence the renal 

203 

clearance, related to Pb in plasma was 

5.8 x iQ"6 x 2740 

2.4 x io"3 x 0.47 

= 14 ml/min. 

Harrison et al. (1966) found (plasma) renal clearance rates (1 to 8 days after injection) of 2.4, 7.6, 7.1 and 2.4 ml/min for radioactive isotopes of Ca, Sr, Ba and Ra 

respectively. 

-93-
TABLE 8.1 

203 Excretion of Pb following intravenous saline injection 

1977 series 

Subject 

ACC (1) 

(2) 

DN (1) 

(2) 

PL 

ACW 

MJH 

ANBS 

Mean 

S.D. 

C V . 

203 

Percentage of injected Pb 

excreted per day 

(period 3-14 days) 

U 

0.90 

0.83 

0.81 

0.85 

0.72 

0.78 

0.92 

0.87 

0.83 

0.07 

8% 

F

e 

0.50 

0.61 

0.34 

0.39 

0.36 

0.19 

0.58 

0.31 

0.41 

0.14 

34% 

Vu 

0.56 

0.73 

0.42 

0.46 

0.50 

0.24 

0.64 

0.36 

0.49 

0.15 

33% 

TABLE 8.2 

Comparison of endogenous fecal and urinary excretion 

in different series of experiments 

Subject 

ACC 

MJH 

DK 

Mean 

Fe /U 

203 Percentage of initia l Pb 

excreted per day 

(period 3-14 days) 

Saline injectio n 

1974 and 1977 

U 

0.9 0 

0.83 

0.9 2 

0.81 

Fe 

0.50 

0.61 

0.58 

0.34 

0.85 ; 0.39 

i 

i 

1 0.86 0.48 

0.56 

Inhalation 

1973 - 1977 

U 

0.62 

0.48 

0.66 

0.83 

1.23 

1.01 

1.30 

0.89 

0.72 

0.63 

0.66 

F

e 

0.56 

0.66 

0.46 

0.59 

0.56 

0.66 

0.66 

0.40 

0.32 

0.40 

0.53 

0.61 

-94-
T T""'w T

T r 

TABLE 8.3 

203, Accounting for Pb in saline injections (1977 series) 

a ii: J 503 

The sum of whole body, fecal and urinary Pb as a percentage 

of the quantity injected 

DAY 

1 

2 

3 

4 

5 

6 

7 

8 

9 

10 

11 

12 

13 

14 

Subject 

MEAN 

OVERA LL MEAN 

ACC, 

100.2 

98.4 

97.7 

98.9 

98. 3 

96. 8 

94. 4 

97. 8 

ACC2 

99. 8 

96. 0 

96. 7 

93. 0 

93. 3 

95. 8 

W

l 

99. 2 

100.0 

100.0 

97. 7 

98. 0 

98. 3 

101.0 

102.4 

99.6 

DN2 

102.1 

103.4 

101.4 

100.9 

105.4 

113.7 

86.4 

101.9 

9 9 . 

MJH 

100.0 

98. 0 

97.6 

99. 5 

102.9 

95. 1 

102.4 

99. 4 

7 

ANBS 

100.2 

101.4 

102.2 

99.7 

103.1 

107.2 

102.3 

PL 

99.2 

99.5 

97.9 

98.0 

98.6 

97.0 

97.6 

105.7 

99.2 

ACW 

99.6 

99.5 

99.0 

100.8 

101.0 

101.4 

102.3 

109.9 

101.7 

TABLE 8.4 

203 Urinary and fecal excretion of Pb relative to concentrations 

in whole blood following injection 

Mean 

S.E. 

Subject 

ACC (1) 

AOC (2) 

DN (1) 

D\i (2) 

PL 

ACW 

MJH 

ANBS 

Blood 

mass 

(g) 

4100 

4100 

5500 

5500 

5000 

5500 

5700 

5600 

Renal 

clearance 

(g/h) 

3.78 

3.46 

4.05 

4.16 

3.45 

3.89 

3.54 

4.26 

Fecal 

clearance 

(g/h) 

2.08 

2.54 

1.62 

1.91 

1.73 

0.85 

2.25 

1.52 

Total 

clearance 

(g/h) 

5.86 

6.00 

5.67 

6.07 

5.16 

4.74 

5.79 

5.78 I 

Blood mass 

Total clearance 

(h) 

700 

683 

970 

90S 

965 

1160 

984 

969 

Clearance 

half-lif e 

(d) 

20.2 

19.7 

28.0 

26.2 

27.9 

33.5 

28.4 

28.0 1 

3.82 

0.11 

1.62 

0.16 

5.64 

0. Hi 

-95-
P.97 

TABU 8. 5 

203„ Comparison of the observed biological half-lif e of Pb 

blood with the calculated {Fc + U) half-lif e from Table 8.4 

Subject 

AOC 

DN 

PL 

ACW 

MJH 

ANB5 

No. or 

observations 

2 

2 

1 

1 

1 

1 

Half-life (T^) (d) 

Observed 

15.5 

22.2 

22.8 

21.6 

16.2 

13.9 

Calculated (Ffi + U) 

20.0 

27.1 

27,9 

33.5 

28.4 

28.0 

Mean 

Ratio 

1.29 

1.23 

1.22 

1.55 

1.75 

2.01 

1.51 

TABLE 8.6 

203, Relation between Pb in urine and plasma, 0-46 hours 

Saline Injections 1977 

Subject MJH 

Period 

0-0.5 

0.5-1.0 

1.0-1.5 

1.5-2.0 

2.0-2.5 

2.5-3.0 

3.0-3.8 

3.8-4.7 

4.7-6.1 

6.1-7.6 

7.6-9.6 

9.6-16.5 

16.5-18.5 

18.5-20.5 

20.5-24.3 

24.3-27.5 ! 

27.5-35.5 i 

35.5-45.5 

203Pb in plasma 

nCi/lnl 

1.26 x io" 2 

3.74 x io" 5 

2.40 x IO- 3 

2.00 x iO"3 

1.72 x IO"3 

1.52 x 10"S 

1.35 x 10~3 

1.22 x IO"3 

1.07 x IO"3 

9.5 x IO"4 

8.6 x IO" 4 

6.8 x IO" 4 

6.2 x IO" 4 

5.7 x IO"4 

5.2 x IO" 4 

5.0 x iO"4 

4.8 x io" 4 

4.2 x iO" 4 

20 % 

* P b in urine 

nCi/h 

30.9 

17.7 

13.7 

6.74 

4.86 

3.09 

1,18 

1.02 

1.38 

1.48 

1.63 

0.72 

0.98 

1.24 

0.98 

0.74 

0.85 

0.89 

Volune of plasma 

cleared of 203pb 

per min 

40.9 

78.9 

95.1 

56.2 

47.1 

33.9 

14.6 

13.9 

21.5 

26.0 

31.6 

17.6 

26.3 

36.2 

31.4 

24.7 

29.5 

35.3 

-96-
P.98 

3 

O 

C l 

Oi 

c 

u 

X 

0> 

o 

a 

3 

aV 

o> 

o 

c 

« l 

u 

L. 

4/ 

a. 

12 16 20 

Hours elapsed 

AERE. R9198. FIG. 8.1. RATES OF EXCRETION OF 203 Pb IN URINE DURING 

THE FIRST 34H0URS FOLLOWING INTAKE 

-97 -
P.99 

^ 1 

9 

O 

£. 

%m 

a 

c 

tm 

3 

c 

•o 

u 

JC 

o 

OL 

a. 

f> 

o 

rsi 

* 

a 

c 

u 

a 

a. 

0 01 

12 16 20 

Hours elapsed 

A.E.R.E.R9198. FIG 82 . RATE OF EXCRETION OF

 203Pb IN URINE DURING 

THE FIRST 36H0URS AFTER INH A L ATION. C OMPARI SON OF ti ) FIV E 

DIFFERENT AEROSOLS FOR ONE SUBJECT. I.i) FOUR DIFFERENT 

SUBJECTS FOR ONE AEROSOL. 

-98-
P.1 

i-fT^'^'wri* 

3 0 

2 0 

o 

a. 

10 

i r 

3 0 

2 0 

10 

i 1 1 1 1 r 

INHALATIONS 1973/74 

x Urine 

• Fatcti 

i r 

I 1 1 L 

1 V. SALINE INJECTIONS 1977 

i r 

^-i—h 

J L 

i—I' 

I 1 I I I I L 

A E 

t 5 6 7 6 9 10 11 12 13 U 

Ooy* 

RE R9198 FIG 6 3 EXCRETION OF

 203Pb IN URINE AND FAECES FOLLOWING (o l INHALATION OF HQTQR 

EXHAUST AEROSOLS AND Ib l I V INJECTION OF

 Z03 PbCt ? 

-99 -
? 

9 0 -

80 

J* 

0 . 

o 

o 

<N 

M_ 

O 

TJ 

« k 

O * 

u 

o 

E 

o 

Q. 

*o 

C 

E 

2: 

E 

70 

60 

50 

40 

30 

20 

10 

0 1 

T 1 I r 

w Soling injection (1) 

— — — Mean of 7 inhalations 

— -—Ingestion , fasting (1 ) 

1 1 

0 5 1 10 50 100 

Hours elapsed 

A.E.R.E.R9198. FI0.84. EXCRETION OF

 203Pb IN URINE EXPRESSED IN TERMS OF BLOOD PLASMA 

2 0 3

 Pb. COMPARISON OF INTRAVENOUS SALINE INJECTION AND INHALATIO N . , 
P.3 

203 

9.- Ingestion experiments with Pb 

9.1 Object of experiments 

Most people ingest much more lead than they inhale, but tin: percentage uptake 

from the gut is often quoted as about 10% whereas the Inhalation experiments with 

Pb show that uptake from the lung is virtually complete. The figure of 10% 

uptake from gut is however not very securely based, and several lines of evidence, 

reviewed in Section 10 below, suggest that the percentage uptake may be higher. 

203 

Some measurements of uptake from gut were therefore made with Pb. A detailed 

study of the effect of diet on uptake of lead was not attempted, but an attempt was 

made to estimate the range in normal subjects by measuring uptake under four 

conditions 

(a) soluble lead (PbCl,) taken after fasting overnight, 

(b) soluble lead taken with a meal, 

(c) insoluble lead (PbS) taken fasting, 

(d) insoluble lead taken with a meal. 

A panel of 6 adult male subjects took part in this comparison. A few measure203 ments were made of uptake of Pb by subjects who swallowed filters which had 

collected exhaust aerosol. 

9.2 Methods 

203 

PbCl„ with 75 ue stable PbCl, carrier was administered in 100 ml of water. 

203 

PbS was precipitated from chloride solution by rUS, separated by filtration through. 

an AA millipore disc and washed with distilled water. A small segment of the filter 

203 

paper, carrying an appropriate amount of Pb and about 50 ug carrier was swallowed 

with water. No food was taken for 12 hours before the fasting ingestions nor for 

203 2^ hours afterwards. For ingestion with food, the Pb was swallowed in the course 

of a late breakfast. This was a standardised meal of bread, cheese, boiled egg, 

milk and an apple. 

203 The activity of Pb ingested was suited to the anticipated uptake and ranged 

from 1 to 5 LCi. Before ingestion, the activity of Pb to be administered was 

measured, and all vessels were checked for residues afterwards. 

t

ycw 

The amount of Pb in the subject's body 5 days after ingestion was measured 

in the 'whole body' counter. This is an array of six sodium iodide crystals 

arranged above and below the supine subject. To confirm that enough time had 

203 elapsed for excretion of unassorted Pb, the measurement was repeated on the 6th 

203 

and 7th days. The Pb in venous blood samples, and in excreta, was measured as in 

other series of experiments. 

9.3 Uptake from the gut 

The observed uptakes ranged from 2% to 60% (Table 9.1). The presence of food 

reduced the average uptake of PbCl, by a factor of 6.5 but the effec t was less marked 

for PbS (factor 1.8). The uptake of PbCl- was greater than that of PbS by a factor 

-101-
P.4 

of ».8 fasting but only by a factor of 1.2 with food. The presence of food, by 

incroeMh* ability in th* tu*meh, night mnlu- Pvi mer* soluble •nd available for 

uptake. 

In Table 9.2 results of the present work are compared with results of Wetherill 

et al. (1975) who used a stable isotope technique to estimate uptake. The results 

203 

of Blake (1976) who gave oral doses of PbCl. to subjects between meals, are also 

given. There is a single experiment of the latte r type in the current work which 

compares well. The main discrepancy is in the uptakes observed Tor lead sulphide 

under fasting conditions where Wetherill et al.'s value is similar to that for 

chloride, whereas the Harwell value is lower by a factor of 4. 

In Fig. 9.1 the percentage uptake for each compound is plotted in terms of the 

mode of intake. It is clear that subjects with high uptake in one mode tend to 

have a high uptake in the other node and that for PbCl, the correlation is good. 

Table 9.3 shows the hierarchy of subjects arranged according to the order of their 

percentage uptake. Comparison of the sets (a) and (b) shows that the hierarchy is 

nearly the same whether uptakes fasting and with food are considered separately or 

taken together by averaging the percentage uptake fasting and with food. The 

analysis of the positions of the subjects in set (a) shows that the order is not 

random. If some subjects consistently take up a higher percentage of ingested lead 

than others, this will explain the variation in blood lead of people exposed to 

similar levels of lead in food, drink and air. 

The additional measurements with exhaust aerosols are summarised in Table 9.4 

an! are compared with earlier measurements. In the environment the route by which 

exhaust aerosol enters man's diet might, in part, be due to actual aerosol material 

contaminating vegetation, surfaces and utensils (to which the data in Table 9.4 are 

relevant) or might, in part, be due to the uptake of the lead by vegetation and its 

incorporation into plant tissue . The lead might then be In a chemical form which 

resulted in different levels of uptake. Experiments to explore this proved impossible because the low uptake of lead by the plant systems combined with the short 

half-lif e of the Pb did not permit production of adequate quantities of labelled 

material for this type of experiment. 

A single ingestion experiment was undertaken using precipitated PbCrO-. 

This was of interest because i t is an extremely insoluble compound. It is however 

slightly soluble in HCl. The observed solubilitie s of the labelled compound were:-

0.45% HCl 0.88 Ug/ml 

0.05% HCl 0.20 ug/ml 

distilled water 0.012 ug/ml 

203 One subject (MJH) ingested 2.3 uCi of PbCr04 associated with 90 ug or stable 

lead as chromate immediately before a normal midday meal. The observed uptake was 

14% (a typical value for unspecified compounds and dietary states). This represents 

13 ug or lead. Assuming the solubilitie s given above and a stomach acidity (with 

food) equivalent to 0.15% free HCl, 13 ug of Pb would require a volume of only 35 ml 

-102-
P.5 

so that the obse- t upt <•.•.'•;« of this salt, popularly regarded as insoluble, is not 

unreasonable. 

It is dii"fi'V : to Ci-ive a mean percentage uptake of dietary lewd from tin-

?03 results with ' i>b. This will depend on the chemical nature or the lead in the diet. 

The results in fasting subjects may mean thnt lead uptake is inrticularly high when 

lead is ingested in water and beverages, taken without food. 

If i t is assumed that a person is in balance for lead, the uptake from gut and 

lung together should equal the urinary and endogenous fecal excretion. In the 

balance experiments or Kehoe (1961b), daily oral doses or lead were given and the 

contribution or air lead to the total intake was small. In Section 10.2, Kehoe1s 

data are re-examined with the additional assumption that the ratio F Ai of endogenous 

fecal to urinary excretion had the same value of 0.5 in Kehoe's as in the AERE subjects (Section 8.4). With these assumptions, the average uptake of lead Tram the 

gut by Kehoe's subjects was 15% (Tables 10.2 and 10.3). In UCLA subjects given oral 

204 doses or Pb as nitrate with meals, rather lower percentage uptake was round 

(Table 10.5), but when the dose was taken Tasting uptake was much higher (Table 9.2). 

203 9.4 Observations on absorbed Pb following ingestion 

20 ^ 

9.4.1 Pb in blood 

203 

The Pb in venous blood followed a very similar pattern to that following inhalation or injection. A peak was reached arter 24-48 hours at a mean or 

52% (S.E. 2%) or the absorbed lead in the whole blood volume. The dirrerence 

between Tasting and non-Tasting experiments is not signiTicant, nor is the 

dirrerence between intakes or PbCl„ or PbS. 

In the early stages or uptake the dirrerences in blood levels are signiTicant (Fig. 9.2). Following ingestion or PbCl, whilst Tasting the appearance 

203 

oT Pb in blood was slightly delayed relative to that Trom PbO in lung but 

reached similar levels arter 4-5 hours. However when PbS was taken with food 

the delay was more marked and equivalent levels were not reached until 24 hours 

had elapsed. A similar delay was present in the plasma levels which are normally at their highest immediately arter intake. This was only observed in the 

Tasting experiments, the lower uptake in the presence oT Tood making plasma 

determinations extremely inaccurate. The peak level in plasma appears to be 

delayed by 1-2 hours. 

ATter the peak concentration in the blood had been reached the blood level 

declined in the normal way with a single exponential. The halT-liTe was determined in rive cases (Table 9.5) involving three subjects. The mean halT-liTe 

or 15.4 d with S.E. 2.7 d does not diTTer signiTicantly Trom the inhalation case 

although the Pb entered the blood via the portal instead oT the pulmonary 

circulation. 

9.4.2 Appearance oT systemic lead following ingestion 

On one occasion, following ingestion oT PbS with Too.l, s.ysi.miit l»-ml, 

as indicated by Pb present in the legs, was monitored to eomjure the changes 

•103-
P.6 

with those observed in lung clearance experiments. The observations showed a 

rise to a peak level at 24 hours followed by a slow decline, similar to that of 

203 

Pb in blood. However, as might be expected from the observations on blood 

203 

and urine, the initial increase in Pb concentration was delayed but achieved 

a peak after a period of 40 h. In Fig. 9.3 the data are compared with those 

203 obtained from Pb(NO-)2 inhalations. The comparison is therefore between the 

most rapid lung uptake with the lowest (and probably slowest) type of gut uptake. 

It was not possible to make an accurate absolute comparison (i.e. in terms of 

203 Y counting rate per uCi Pb) because the need to shield the detector from the 

relatively massive amount of Pb in the subject'6 gut affected the counting 

efficiency, but at the peak (at 24 hours) the observed specific counting rates 

agreed to within 20%. 

9.4.3 Excretion 

Some reference to early excretion following ingestion has been made in 

Section 8. At a later period (5-7 days post intake) the mean level of Pb 

in urine, expressed as a percentage of uptake, was 1.08 1 0.08% (S.E.) per day 

(4 subjects) when fasting at intake and 0.96% per day (t subject) for intake 

with food. This compares with 0.83,1 0.03% per day following saline injection. 

The fecal excretion rate was 0.86 1 0.14% per day (3 subjects) compared with 

-. 0.41 1 0.05% per day following injection. This suggests that even after 6 days 

there stil l may be some residual passage of non-absorbed Pb from the gut. 

If so the associated error will be quite small because an excess of 0.4% of 

uptake per day corresponds to a mean value oT 0.08% oT intake per day (assuming 

20% uptake) for a limited period. 

In four cases a complete collection of urine and feces was undertaken, and 

at 7 days post intake, the maximum quantity of Pb not accounted for by 

excretion and whole body counting was 5.3% (mean value -1.6%). 

9.5 Summary- of results oT ingestion experiments 

Uptake of lead from the gut is affected both by the chemical form of the lead 

and by the presence of food in the stomach. Both efTects are important and must 

be considered against a background oT marked and consistent subject-to-subject variation. It appears probable from this work that the effective mean percentage uptake 

for healthy males lies in the range 13% to 18%. Once the lead is absorbed into the 

system it behaves essentially as that derived from injection or inhalation except for 

an initial delay in uptake of a few hours which is greatest for insoluble lead in the 

presence of food. 

-104-
TABLE 9.1 

203 

Percentage uptake oT Pb Trom the gut 

P.7 

Subject 

ACC 

MJH 

ACW 

DHFA 

DN 

KFB 

Mean 

S.D. 

S.E. 

Percentage uptake Trom 

the gut 

Fasting 

PbCl2 

54 

40 

60 

28 

65 

24 

45 

17 

7 

PbS 

26 

2 

13 

2 

9 

20 

12 

10 

4 

With 

PbCl2 

11 

6 

6 

4 

11 

5 

7 

3 

1 

food 

PbS 

8 

5 

7 

3 

8 

5 

6 

2 

1 

Mean 

25 

13 

22 

10 

23 

14 

18 

6 

3 

Fasting 

Food 

PbCl2 

4.9 

6.7 

10.0 

7.0 

5.9 

4.6 

6.5 

1.9 

0.8 

ratio. 

PbS 

3.3 

0.3 

1.9 

0.5 

1.1 

4.0 

1.9 

1.9 

0.8 

TABLE 9.2 

Percentage uptake oT lead Trom the gut: comparison 

oT published data 

' 

Author 

Wetherill et al. (1975) 

Present work 

Blake (1976) 

Present work 

Percentage uptake 

Trom gut 

With Tood 

— 

9.5 (3) 

6 (6) 

7 (6) 

Fasting 

35 (3) 

34 (3) 

12 (6) 

45 (6) 

21 (11) 

20 (1) 

Lead compounds used 

PbS 

Pb(N03)2 

PbS 

PbCl2 

PbCl, between meals 

«i II it 

(Figures in brackets are the number oT observations) 

-105-
I 

i 

(a) 

TABLE 9.3 

203 The hierarchy oT subjects in Pb Ingestion experiments 

(b) 

Posi tion 

in 

hierarchy 

1 

2 

3 

4 

5 

6 

Fasting/with food 

considered separately 

PbCl2 

Fast 

DN 

ACW 

ACC 

MJH 

DHFA 

KFB 

Food 

DN 

ACC 

ACW 

MJH 

KFB 

DHFA 

PbS 

Fast 

ACC 

KFB 

ACW 

DN 

DHFA 

MJH 

Food 

ACC 

DN 

ACW 

MJH 

KFB 

DHFA 

Fasting/with food 

considered together 

PbCl2 

DN 

ACC 

ACW 

• 

MJH 

DHFAI 

KFB 

PbS 

ACC 

DN 

ACW 

KFB 

t 

1 

MJH 

DHFA 

(c) 

Mean position in 

hierarchies under (a) 

Subject 

ACC 

DN 

ACW 

MJH 

KFB 

DHFA 

Mean 

1.75 

2.00 

2.75 

4.25 

4.50 

5.75 

± S.E. 

0.48 

0.71 

0.25 

0.25 

1.36 

0.25 

(Brackets indicate close 

grouping) 
P.9 

TABLE 9.4 

203 Percentage uptake in gut oT Pb-labelled exhaust 

aerosols 

Subject 

ACC 

MJH 

ACW 

DHFA 

DN 

1 

Clean 

exhaust 

69 

-

51 

11 

-

1977 

r

asting 

Carbonaceous 

exhaust aerosol 

35 

16 

-

40 

-

1973 

Between meals 

UnclassiTied 

exhaust aerosol 

8 

9 

-

-

16 

TABLE 9.5 

Hair-llTe in blood oT Pb following ingestion 

compared with values following saline injection 

Subject 

MJH 

DN 

ACC 

Mean 

HalT-liTe 

d 

13.5 

14.4 

22.3 

10.5 

15.3 

15.4 t 6. 0 S.D. 

2.7 S.E. 

Saline injectio n 

halT-liTe 

d 

14.9 (1974) 

17.4 (1977) 

22. 0 (1974) 

20.9 (1977) 

23.2 (1977) 

13.9 (1974) 

15.3 (1977) 

15.7 (1977) 

-107-
P.10 

X PbCt2 

PbS 

c 

til 

o 

in 

a> 

o 

o. 

o> 

o> 

o 

c 

a> 

u 

k. 

c> 

0. 

2345678 9 10 

Percentage uptake with food 

A.ERE . R9198. FIG. 9.1. PERCENTAGE UPTAKE FROM THE GUT OF 

203 PbC!2TAKEN WITH AND WITHOUT ACCOMPANYING FOOD 

-108-
I 

§ 

Of 

E 

O 

> 

o 

o 

o 

SI 

J3 

0 . 

m 

o 

CM 

a> 

JO 

t. 

o 

</) 

x> 

o 

Ot 

at 

o 

c 

a> 

o 

i_ 

o> 

CL 

100 

1 0 -

PKHO Injection 

SUBJECT ACC 

JOJLA 

1 10 10 100 

Elapsed hours 

A ERE R9198 FIG 9 2 VARIATIONS OF LEVEL OF

 203 P b IN WHOLE BLOOD FOR VARIOUS MOOES 

OF INTAKE. 
P.12 

l/l 

z 

o 

< 

o 

z 

< 

z 

o 

UJ 

o 

z> — 

o 

£ o 

z 

TJ — 

O _ | 

UJ 

o 

u. 

in 

o 

(M73 »D) s6a | ui AI;A!)3D >)Ddd jo e6o)ueDjed 

Cv 

O 

O 

CM 

ci 

oi 

O 

u. 

CO 

o> 

en 

or 

ui 

cc 

ui 

< 

-110-
P.13 

10. Synthesis oT AERE and other results 

10.1 Introduction 

In this section published studies on the uptake, distribution, retention and 

excretion oT lead are evaluated and related to the Tindings oT the Harwell work. 

Also, the available evidence is examined on same issues which could not be studied 

directly, such as the response oT children's blood lead to lead in air and the 

relative intakes Trom air, water and diet. 

It is almost impossible to review the extensive, and not wholly consistent, 

literature on human uptake or lead without introducing some element or personal 

choice or discrimination. The objective oT this section is to examine how Tar a 

consistent picture can be built up which encompasses most oT the major published 

contributions. 

The Tollowing abbreviations are used: 

PbA 

PbB 

PbU 

PbW 

APbB 

A 

I 

til 

G 

U 

F 

fg " 

•gh " 

fs " 

ab 

Concentration oT lead in air (ug/m ) 

Concentration oT lead in blood (ug/iOO g) 

Concentration oT lead in urine (ug/l) 

Concentration or lead in water (ug/l) 

Increase in PbB due to exposure to PbA or PbW 

Lead deposited in lung (ug/d) 

Lead ingested in rood and drink (ug/d) 

Increase in I due to oral doses 

Lead taken up Trom gut (ug/d) 

Lead excreted in urine (ug/d) 

Lead excreted in Teces (ug/d) 

Endogenous Tecal excretion (ug/d) 

Lead stored (ug/d) 

G/I Tractional uptake Trom gut 

Fraction oT uptake from gut which is transferred to red cells 

S/G fraction of uptake which is stored 

f f fraction of ingested lead which is stored 

Mass of blood (kg) 

Fractional deposition in lung 

Fraction of lung burden transTerred to red cells 

Biological halT-liTe in blood (days) 

The published inTormation is or three main types: 

-111 -
• r'rT-.uriP.14 

(a) Population surveys in which PbB of individuals or groups OT p; • «ons are 

correlated with locally measured PbA. 

(b) Experiments in which volunteers are exposed to artificially enhanced PtiA 

Tor a number oT hours per day over long periods and the resulting variations in PbB measured. Alternatively, PbA may be eliminated by keeping 

volunteers in clean air environments and the consequent decline in PbB 

observed. 

(c) Studies or the lead balance oT individuals, in which the contributions 

oT lead in rood and drink are assessed, and the contribution or PbA 

estimated. 

The dirTiculty with population surveys is that or uncontrolled variables. 

Numerous surveys have shown correlations oT PbB and PbA in diTTerent areas or cities, 

or depending on distance Trom some known lead sources, but very oTten there is the 

possibility that Tactors such as housing, occupation, dietary and social habits may 

also contribute to the observed gradients in PbB. A comparison or the PhBAbA 

203 relation deduced Trom work with Pb with the results oT two major population surveys 

was made in the previous paper (Chamberlain et al. 1975). Some Turther references 

to this type oT survey are given in this paper, and a full review has been published 

by Bridbord (1977). 

It is considered worthwhile to re-examine some oT the main published work oT 

types (b) and (c) above in the light oT the information obtained with 

is done in relation to: 

203, Pb. This 

(i) Estimates oT Tractional uptake oT lead in air and diet, and transTer and 

retention in blood, skeleton and other organs. 

(ii) Relationship between PbB and PbA. 

(iii) Relative contributions oT lead in air, rood and water to total intake. 

10.2 Uptake and storage oT lead in Kehoe's experiments 

Kehoe (196lb) gave daily oral doses oT Pb to subjects, analysed diet, urine and 

feces, and drew up balances of ingested and excreted lead Trom which the amount stored 

was estimated. 

The results shown in Fig. 11 oT Kehoe (1961b) are tabulated in Table 10.1. 

Subjects SW, MR and EB, who received respectively 0.3, 1 and 2 ng oT Pb daily, stored 

between 0.05 and 0.08 oT the total lead ingested (oral dose plus lead in diet) over 

the experimental period. Subject IF who received 3 mg/d for 112 d, stored no less 

than 0.15 (15$) of his total ingested lead. 

IT it is assumed that the subjects were in balance as regards normal dietary lead 

with equal amounts transferred to and Trom storage, and the storage during the experimental period related solely to the oral dose, then this represents a Traction T 

s 

oT the dose equal to 0.08 to 0.09 Tor subjects SW, MR and EB and 0.16 Tor IF. 

IT f is the fractional uptake in gut, and f the fraction of the uptake transferred to storage, then Kehoe's results give a measure of the product f = f r . 

s g gs 

-112-
P.15 

As will be 

the ratio : 

;7Wn , T and f can be deduced separately IT an assumption is made about 

© ©^ 

or endogenous Tecal to urinary excretion. BeTore doing that, it Is 

worth noting that values or f of about 0.08 are consistent with f_ about 0.16 (i.e. 

s g 

\S% uptake from gut) and f about 0.5 ( i.e . 50$ oT absorbed lead transTerred to 

gs IT T is less than 0.5, then T must be more than 0.16, and vice versa, 

gs g 

storage). 

Moreover, Kehoe's estimates or stored lead reTer to the net storage over the experi 

mental period, which in MR's case was as long as 1456 days. 

For subjects MR and EB, Kehoe gave a detailed analysis or daily intake, excretion and storage of lead, which is reproduced in the upper part oT Table 10.2. Kehoe 

noted that Tor both subjects, the amount oT lead stored was oT the same order as the 

amount excreted in urine. It was not possible to assess the endogenous Tecal excretion during the period oT oral dosing, since it was masked by the relatively larger 

amounts oT unabsorbed lead excreted in Teces. By comparing the Tecal excretion oT 

the subjects during the follow-up periods (also shown in Table 10.2) with the Tecal 

excretion of the same subjects before dosing began, Kehoe (196lb, Tables 22 and 23) 

obtained estimates (necessarily approximate) that subject EB's endogenous Tecal 

excretion was about equal to his urinary excretion whereas subject MR's endogenous 

Tecal excretion was small. 

IT a Tigure is assumed Tor F AJ, the true uptake Trom the gut in Kehoe's subjects can be deduced, 

assumptions 

In the lower part of Table 10.2 this is done with the 

(a) F /\J =0.5 Tor both subjects (this is the mean value Tor the Harwell 

(b) Fe/U 

subjects), 

1 Tor EB but F Aj = 0 Tor MR. 

On assumption (a), the fractional uptakes Trom gut, T , during the dosing 

period, are 0.14 (MR) and 0.15 (EB). On assumption (b) they are 0.11 (MR) and 0.18 

(EB). The Traction, f , oT the uptake which are stored are 0.40 and 0.50 on the 

gs 

Tirst assumption and 0.49 and 0.43 on the second. 

Thus Kehoe's very lengthy and detailed analysis oT the lead balance oT these 

subjects implies that between 0.11 and 0.18 oT oral doses oT lead were absorbed, and 

0.4 to 0.5 oT the absorbed dose was stored Tor periods oT months to years, presumably 

mostly in bone. 

In Table 10.3 a similar calculation is done Tor Kehoe's subject PC, who was 

exposed Tor 37.5 hours per week Tor 88 weeks to an aerosol oT 150 ug/m oT lead oxide 

in an experixnental chamber. Kehoe estimated that the retention oT the aerosol in 

the lung was X% and that the total amount oT lead deposited in the lung was 98 mg. 

This is consistent with a 10 1/min ventilation rate in the lung. As the aerosol wag 

sub-micron in size , i t is assumed that the deposition was in the pulmonary region, 

and that all the retained lead was taken up into the circulation, with negligible 

amounts removed by ciliary action and swallowed. 

The analysis or the data Trom subject PC, with the assumption that F A) c 0.5, 

gives 0.19, 0.12 and 0.21 Tractional uptake rrom gut in the preliminary, experimental 

-113-
P.16 

and follow-up periods respectively. During the 616 days or the ev.\ 2.\Litiental period, 

i t is estimated that FC took up 16.5 mg Pb Trom his gut, making, 'M.th v,he 98 mg 

retained in the lung, a total intake oT 114.5 mg. The net amount j-ci-ed was 47 mg, 

\j which is 0.41 or the total uptake or 0.48 oT the amount retained in the lung. 

The conclusion Trom this re-examination or Kehoe's results is that they are 

203 consistent with the hypotheses, derived Trom work with Pb 

(a) Uptake from gut is about 15-20$ of ingested Pb, 

\ (b) About hair the uptake becomes Tixed in blood and is excreted with a 

halT-liTe oT about 20 days, 

\ (c) Most or the other hair is stored in bone or elsewhere with a halT-liTe 

oT order years. 

10.3 Uptake and storage oT lead in UCLA experiments 

Rabinowitz and his colleagues at University or CaliTornia, Los Angeles (UCLA), 

204 did a notable series oT experiments in which the stable isotope Pb was given to 

subjects orally (Rabinowitz, 1974; Rabinowitz et al. 1973, 1976a, b, 1977; 

Wetherill, et al. 1975). In some experiments the subjects were Ted a low-lead diet 

during the experimental period, so that the total lead intake (diet plus oral dose) 

204 

was unchanged. Mass spectrometry was used to determine the amount oT Pb in blood 

and excreta. Also, in two subjects, bone biopsy samples were taken Trom the ilia c 

crest to measure the uptake by bone. 

The total lead content of biological samples was also determined by mass spectro208 metry, using the isotope dilution method in which a spike of Pb wa6 added to the 

samples. This method is independent of the yield or the chemical analysis step. 

A very high degree of accuracy was obtained. Replicate analyses of homogenised 

fecal samples agreed to within 2$ (Rabinowitz et al. 1977). 

Sequential sampling oT blood every Tew days gave curves which suggest random 

errors or order 1#. This high degree or reproducibility enabled Rabinowitz et al. 

to observe the eTTect on blood lead oT putting a subject in a clean-air room. 

Rabinowitz et al. interpreted their results in terms oT a three-compartment 

•odel, with the first compartment blood, the second sort tissue and the third bone. 

There are two diTTerences between the UCLA and Harwell models. In our view, blood 

plasma and red cells must really be considered as two compartments. The initia l 

uptake or Pb Trom lung or gut is to plasma, where i t is rapidly distributed to red 

cells, bone and other storage sites. While there may well be transTer to and Tro 

between blood, bone and other organs at later times, the initia l distribution appears 

to be achieved within the Tirst Tew hours. In the UCLA model, Pb entering blood has 

a mean residence time there oT about 36 days, and is then excreted in urine, transferred to bone, or transferred to a second soTt tissue pool. In the second pool, 

the residence time is about 40 days. Endogenous Tecal excretion (in bile , gastric 

secretions and pancreatic secretions) takes place Trom the second pool only, and 

consequently is delayed by about 40 days relative to urinary excretions. 

-114-
P.17 

The method oT measuring s ogenous Tecal excretion by the UCLA workers during 

2D4 

the period or dosing with Pc, was as Tollows (Rabinowitz, 1974, p.10): "Alimentary secretion collections were made with a dual rubber tube passed orally and 

located with a Tluoroscope. A slight vacuum was applied. Basal resting gastric 

collections were made, then cholecystokinin was used to induce bilary flowagc, and 

204 later secretin stimulated pancreatic Tluid production". The Pb and total lead 

concentrations were measured in the samples so obtained, and the daily output 

derived using standard estimates oT volume or bile etc. produced each day (Rabinowitz, 

1974, Table VIII). 

204 During the Tollow-up periods arter the oral doses oT Pb were discontinued 

204 

Pb in Teces could be attributed unambiguously to endogenous excretion. The 

results ( Rabinowitz et al. 1976b) are shown in Table 10.4. The mean endogenous 

Tecal clearance (F /PbB), was 2.5 g/h» compared with 1.8 gAi in the Harwell subjects 

receiving Pb by injection (Table 8.4). 

The diTTerence between the Harwell and UCLA Tindings is in the time or onset 

oT endogenous Tecal excretion. Harwell work with Pb, and also work with Pb 

212 

or Pb on baboons (Cohen, 1970), dogs (Lloyd et al. 1975) and rats (Morgan et al. 

1977) indicates that endogenous Tecal excretion is established almost simultaneously 

with urinary excretion, the only apparent delay being due to the time taken Tor 

passage or Tecal matter. This also appears Trom the experiments oT Harrison et al. 

(1966), and Harrison and Sutton (1967), in which Ca, Sr, Ba and Ra were 

injected into human subjects. 

An attempt is made here to assess the UCLA data independently or the UCLA 

model, and also to see the consequences oT applying the Harwell model to the UCLA 

data. 

204 In Table 10.5 the uptake, excretion and storage oT Pb in the UCLA subjects, 

A, B and D are analysed in the same way as Tor Kehoe's subjects in Tables 10.2 and 3. 

The Tigures in the upper part or Table 10.5 are derived directly Trom the results 

given in the UCLA papers with no additional assumptions. The amounts oT stored lead 

calculated Trom the balance between ingestion and excretion (630 ug Tor A, 630 ug 

204 Tor B) agree well with Rabinowitz et aL's estimates oT the skeletal Pb at the 

times oT the bone biopsies (namely 702 ug Tor A, 674 ug Tor B) , assuming that the 

204 concentrations oT Pb in trabecular and cortical bone oT the skeletons generally 

were the same as the concentrations Tound in the trabecular and cortical fraction oT 

204 the biopsy sample. The amounts oT Pb stored represented between 0.03 and 0.04 

oT the total ingested, which is lower than Tound Tor Kehoe's subjects (0.056 - 0.152). 

To deduce the Tractional uptake Trom the gut in the lower part or Table 10.5, 

an estimate is made oT the endogenous Tecal excretion during the period oT dosing with 

204 

Pb by reference to the data or Table 10.4. This gives slightly higher estimates 

or Fg than in Rabinowitz et aL's own analysis but the eTTect on the estimates oT 

uptake Trom the gut is small. In Rabinowitz's analysis, the values or T are 0.085, 

0.065 and 0.109 Tor subjects A, B and D. 

-115-
P.18 

Returning to Table 10.5, the fractions or the uptake which are stored are 0.4, 

0.5 and 0.4, in good agreement with the results derived in Tables 10.2 and 10.3 Trom 

Kehoe's results, and with the concept that most oT the lead taken up from lung or 

gut which does not became attached to red cells is stored in bone. 

The estimates of uptake of

 204Pb can be related to Rabinowitz et al's (1976b) 

204 data on Pb in blood of these subjects. The measurements for subjects A, B and D 

which show excellent internal consistency, are reproduced in Fig. 10.1. If i t is 

assumed that 5556 or the uptake becomes attached to red cells (Table 7.2), and that 

the elimination or Pb Trom blood can be described in terms oT a rate constant X, then 

204 the predicted Pb in blood in units oT ug/lOO g is 

204D.„ 0.055 G , , . w . PbB = — ^ (1 - exp-Xt) 

where G = rate oT uptake Trom gut (ug/d) 

M = blood mass (kg) 

X = rate constant Tor removal from blood (d~ ) 

1/X = mean lif e in blood (d) 

0.693A = half-liTe in blood (Tj . 

From the results of the UCLA work, values oT rate constant, mean liTe, or 

hair-liTe or Pb in blood can be deduced in three ways: 

(a) by Titting curves oT the Torm a[l - exp(-Xt)] to the increment phases 

204 

oT Pb in blood, 

(b) by Titting curves or the Torm a. exp(-Xt) to the decrement phases following 

the end of the dosing period (Fig. 10.2), 

(c) by taking values of G from Table 10.5 and finding values of X such that 

the equilibrium (plateau) value of PbB as measured experimentally 

(Fig. 10.1) is equal to 0.055 G X-1 M~'. 

Methods (a) and (b) depend only on the shape of the curves in Fig. 10.1. 

204 Method (c) depends on the concentration oT Pb in the subject's blood at equili204 brium. A correction must be applied to the recorded maximum value oT Pb to allow 

for a further slight increase to be expected IT the daily dosing had continued until 

equilibrium was obtained. This correction amounts to 5$, S% and 19$ Tor subjects 

A, B and D respectively. The results for the three methods which are essentially 

independent are given in Table 10.6. Estimates by method (b) only are also given 

204 for subjects C and E, who received Pb for one (C) and two (E) short periods. 

The estimates of mean lif e obtained by Rabinowitz e t al. (1976b) from their model 

are also shown in Table 10.6. 

204 As shown in Fig. 10.1, the Pb in blood of the UCLA subjects A and B 

approached an apparent plateau beTore the end oT the period oT dosing. For subject 

D, the halT-liTe in blood was longer (Table 10.6) and a plateau had apparently not 

been reached when dosing ceased at 82 d. It can be estimated that the true plateau 

204 

Pb concentrations were 7.6, 4.8 and 5.4 ug/iO0 g for the three subjects. However 

-116-
P.19 

204 the ratio oT PbB to total PbB at the plateau was not then equal to the ratio oT 

2WPb oral dose to the total Pb in diet as shown in Table 10.7. From these -/..suits, 

Rabinowitz concluded that only about 55$ oT PbB was derived from current dietary 

uptake, the remainder coming from inhaled lead and from rcsorbed skeletal lead. At 

he clearly recognised, this conclusion depends on the percentage uptake from the gut 

204 

of the Pb ingested as a daily dose (with food) and of the dietary lead being 

identical. 

It is possible to juggle Rabinowitz's results in various ways, but it seems 

probable that an appreciable Traction (perhaps 1/4 to 1/3) oT the PbB in middle-aged 

subjects is derived Trom resorbed skeletal lead. Such a belieT is consistent with 

the view that nearly hair oT the Pb taken up Trom gut or lung goes into storage mainly 

in the skeleton (Tables 10.2, 10.3, 10.5). If this rate of storage continued for a 

liTetime, with no resorption, then the increase of skeletal lead with age would be 

greater than is observed (Section 10.8). 

The UCLA study also included measurements of the reduction or blood lead when 

subjects were kept in clean-air rooms. Subjects B, D and E spent 40, 25 and 40 days 

respectively in Tiltered air rooms (Rabinowitz et al. 1976b, 1977). The interpretation Tor subject B is somewhat complicated because changes in the daily oral doses oT 

isotopically-separated lead also took place during the same period but there seems 

little doubt that PbB of subjects B and E declined by between 1.5 and 2.5 Ug/l00 g 

during 40 days in a clean air environment. Since the ambient PbA was probably about 

/ 3 2 ug/m , this is as expected Tram other work. The detection oT a Tall oT this 

magnitude in individual subjects was only Teasible because oT the very accurate UCLA 

technique Tor measuring PbB. 

The UCLA workers (Rabinowitz et al. 1977) assessed the intake oT Pb by the 

respiratory route by three methods (Table 10.8): 

(a) by an overall lead balance, in which inhaled intake is equated to 

dietary minus Tecal minus urinary lead, 

(b) by assessing the contribution oT dietary lead by the tracer technique and 

attributing the remainder to inhaled lead (it is not clear whether a 

contribution Trom resorbed bone lead was included), 

(c) by measuring the response oT PbB to the clean air environment. 

The results obtained by method (c) are possibly the most accurate. The mean 

intake Tor subjects B, D and E by this method, 13 Mg/d, compares with 15 ug/d, the 

value expected iT the air concentration is 2 Ug/m , breathing rate 15 m /d and 

deposition in lung 50$. 

10.4 Elevation oT blood lead in experimental exposure oT subjects to PbA 

(a) Kehoe's subjects 

Kehoe (1961b, Fig. 21), gives the average concentration oT lead in blood 

oT subject PC in each successive period or 28 days. During the 532 day 

preliminary period berore PC's exposure to PbA in the experimental chamber 

-117-
P.20 

began, his PbB averaged 25.7 ug/lOO g. The concentration in the chamber was 

120 ug/m , and PC spent 37.5 hrs/week in it , so the equivalent 24-hour PbA, 

BE shown in Table 10.9 was 33.5 ug/m . When exposure began, FC's PbB rose 

to 42 ug/100 g within 56 days, but thereafter there was no systematic increase, 

though there were fluctuations of ± 10 ug/l00 g which may have been caused by 

changes in dietary lead or fractional uptake from the gut as well as by factors 

relative to inhalation. The diTTerence between the plateau PbB, averaged on 

the last 504 days oT the total exposure period oT 616 days, and the average 

pre-exposure PbB is termed the elevation APbB and Tor PC this works out at 

16.6 ug/100 g. The ratio APbB/PbA is the Tactor a, which in this case is 0.5. 

Kehoe also gives the daily urinary excretion U. The ratio U/PbB, is 

expressed conventionally in the units ml/h (i.e . the amount or Pb excreted in 

urine per hour expressed as the equivalent blood volume). As an attempt is 

Bade in this paper to standardise as mass units rather than volumetric units, 

renal clearances are given in Table 10.9 in g/h. The renal clearance rate 

rose Trom 3.7 g/h pre-exposure to 7.6 g/h during exposure, which means that U 

increased more than proportionately to the increase in PbB. This is commonly 

found in industrial exposure to lead, and shows that excretion is speeded up, 

presumably with an associated reduction in the mean lir e in the blood. 

In another series of experiments, Kehoe (1966) exposed subjects LD and JS 

to the same air concentration (150 Ug/m ) Tor a varying number oT hours per 

day. During 112 days, they were in the chamber Tor 10.5 hours/week, then 

during another 112 days Tor 21 hours/week, then 112 days at 31.5 hours/week 

and Tinally 112 days at 42 hours/week. Thus the 24-hours equivalent PbA was 

9.4, 18.8, 28.2 and 37.5 ug/m . Kehoe tabulates the subjects' PbB at 28-day 

intervals', each value being the mean of 8 determinations. To allow Tor 

adjustment to the increased PbA, only the PbB Tor the last 28 days in each 

112-day period has been used to calculate APbB (average oT LD and JS) in 

Table 10.9. 

Kehoe then did a further series (subjects NK and SS) with the same system 

of 112 days exposure for varying hours per week but with the concentration in 

the chamber reduced to 10 Mg/m . This was evidently designed to test whether 

exposure at ambient as distinct from industrial atmospheres of PbA would give 

appreciable elevation of PbB. The 24-hour equivalent PbA in these experiments 

increased stepwise from 0.62 to 4.37 Ug/m (Table 10.9). Kehoe's (1966) own 

assessment of the results was as follows: "There appeared to be a slight 

increase in the output of lead in the urine and in the concentration of lead 

in the blood of both subjects as the experiment progressed. The increase was 

irregular, late in putting in its appearance in the case of subject SS, and of 

such slight proportion in both instances, as to be of dubious significance. 

The data reveal trends, however, which would seem to be surTiciently persistent 

to be valid". 

-118-
P.21 

In Kehoe's paper, he mentions that a series or pre-exposure measurements 

were done lasting 29 weeks (NK) and 19 weeks (SS), but the results oT these 

are not given in the paper, whereas the results on the similar pre-exposure 

6eries on LD and SS are given. However, Goldsmith and Hexter (1967), who 

used Kehoe's results, give the mean pre-exposure PbB Tor NK and SS, presumably 

having hBd access to the original data, and these Tigures are shown in 

Table 10.9. Taking the Tinal 28 days oT each 112-day experimental period as 

the plateau, APbB is calculated on the increase above the pre-exposure Tigure. 

As there are only two subjects, and eTrectively one data point Tor each subjec t Tor each PbA value (Kehoe's data points are however means oT eight readings), the APbB and a values show considerable scatter (the scatter is reduced 

slightly , and the mean a Tor the whole series littl e altered, IT the Tinal 56 

days oT each 112-day period is taken as the plateau, giving 2 data points per 

subject per PbA level). It is doubtTul iT the variation oT o between periods 

in Kehoe's experiments, or the dirrerence in mean results between the series 

on LD and JS and that on NK and SS, is significant. The overall mean a Trom 

Kehoe's work (12 determinations) is 1.1 with standard error 0.15. 

(b) GrirTin et aL's subjects 

Kehoe's method was to make very complete measurements on a small number 

oT subjects. GrirTin et al. (1975) exposed larger numbers oT volunteers in a 

room at Dannemora, N.Y., where they remained 23 hours per day. Not all the 

volunteers remained Tor the full term of the experiment. In Table 10.9, the 

results or cohorts, each member or which remained Tor the same time, are 

analysed. 

As in Kehoe's experiments, the lead oxide aerosol was prepared by burning 

tetra-ethyl lead in propane. The particle size was 0.05 to 0.1 urn. In one 

experiment the airborne particulate lead concentration was 10.9 ug/m and in 

another i t was 3.2 ug/m (the corresponding 24-hour equivalent to PbA values 

used in Table 9 are 10.4 and 3.1 ug/m ). Samples taken with an iodized 

carbon 'back-up' Tilter behind the particulate Tilter indicated the presence 

of an additional lead component, equivalent to between 10 and 15$ or the total 

amount oT airborne lead in the chamber. Presumably this was unburnt TEL 

vapour. 

PbB was measured in two weekly samples beTore the Dannemora subjects 

entered the chamber and at either weekly or Tortnightly intervals thereaTter. 

Some measurements or urinary' lead as ug Pb per g total solids in urine are also 

given. Using the standard man's output or 60 g/d solids in urine (ICRP, 1975), 

U in ug/d is given in Table 10.9. The average renal clearance in GriTTin 

e t aL's subjects is 4.5 g/h, which agrees well with the Harwell Pb value. 

GriTTin et al. noted that the mean PbB oT their subjects increased at the 

start oT the exposure, but arter about 12 weeks there was no Turther increase. 

In Table 10.9, PbB from 12 weeks onward has been used to calculate APbB and cu 

The mean value of a is 1.55 ug/100 g per ugA> . This makes^no allowance for 

any possible contribution to PbB Trom the 10 or 15$ oT the lead in the atmosphere which penetrated the particulate Tilter. 

r 

-119 -
An alternative method oT analysis oT the Dannemora subjects is shown in 

Fig. 10.3. Here the APbB Tor each subject at each blood sampling is worked 

out by reference to that subject's pre-exposure PbB, and the results are 

averaged. Curves have been fitted of the form 

B(t) = B (I - exp-Xt) 

where B(t) is the elevation of the subject's PbB above the pre-exposure level, 

B is the plateau elevation value and X the time constant. The best fit is 00

 -1 

obtained with the values of B and X given in Table 10.10. The mean liTe X 

00

 3 

or lead in blood deduced Trom this analysis is 41 days (PbA = 10.4 ug/m ) and 

37 days (PbA = 3.1 Mg/m ) and the corresponding T. values are 28 and 26 days. 

These are longer than Tound in the Harwell work (Tj^ = 18 d) but comparable 

with the UCLA results (Table 10.6). 

(c) Tola's subjects 

A similar analysis oT the elevation oT PbB in industrial workers is shown 

in Fig. 10.4, based on the work oT Tola et al. (1973) who measured PbB in 33 

new entrants to a lead works. The average PbB beTore starting work was 

16.5 ug/ioo g. Arter starting work, PbB rose to a plateau oT 49.0 Ug/i00 g 

arter 60 days. The best Tit to the curve oT APbB against time (Fig. 10.4) 

gives X = 0.072 days' , T, = 10 d. The variation oT APbB with time in Stuik 

and Zielhuis's (1975) subjects, who received daily oral doses oT lead (20 ug/kg 

body weight per day) also indicates a shorter T^ than Tound in the UCLA or 

Dannemora subjects. 

10.5 Surveys oT blood lead versus air lead in various regions 

Tepper and Levin (1975) related the blood lead oT groups oT women volunteers 

in 11 communities to measurements oT air lead at a number oT fixed sampling stations 

in each area. The correlation oT PbB with PbA was signiTicant only at the 10$ 

level, but the results were not inconsistent with the hypothesis that a is about 

unity (Chamberlain et al. 1975). The results oT the survey oT Azar et al. (1975) 

were also consistent with that hypothesis. Tsuchiya et %1. (1975) compared PbB in 

policemen from various areas oT Tokyo with PbA measured in those localities. The 

results are shown in the upper part oT Fig. 10.5. 

The regression oT PbB on PbA is signiTicant at the 10$ level, and the line 

drawn in Fig. 10.5 is the equation 

PbB = 16.4 + 2.4 PbA 

where PbB is in ug/100 g and PbA in ug/m . Thus, IT the relation is considered to 

be causative, and to demonstrate the contribution oT air lead to blood lead, then 

the corresponding value or a is 2.4. Commenting on their results, the authors 

state: "It appears that the blood lead level is related to the air lead level, but 

the air lead level is related to unhygienic, or low social condition. Thus it may 

not be concluded that the blood lead level is related to the air lead level in terms 

oT a cause and eTTect relationship". 

-120-
P.23 

In the lower part or Fig. 10.5, the results are plotted oT a study by 

Tsuchiya et al. (1977) or PbB oT urban and suburban children, 12 to 15 years or age, 

in Tokyo. The diTTerence was greater when only children who had lived in the same 

area Tram 3 years or age were included. These results are plotted in Fig. 10.5. 

The authors concluded that the diTTerence in PbB levels between urban and suburban 

children was most likely due to factors other than lead in ambient air. However 

the possibility of this Tactor being a cause oT the diTTerence could not be categorically denied. 

Johnson et al. (1975) compared blood lead in populations living near a freeway 

in Los Angeles (PbA = 6.3 ug/m ) and in a desert area at Lancaster, California 

(PbA = 0.64 ug/m ). The populations were sampled in age groups I 1-16, II 17-34 

and III 35 years of age and over. The results (arithmetic mean and standard error 

of mean) are given in Table 10.11, together with values of a assuming, once more, 

that PbA is the only variable controlling PbB. The results using geometric means 

were similar. The difTerence in PbB between the two populations is greater Tor 

young people than Tor adults. Grouping males and remains together, and assuming 

a linear relation between PbB and PbA, the results or Table 10.11 suggest 

Adults (groups II & III) : PbB = 9.9 + 0.8 PbA 

Young persons (group I) : PbB = 9.5 + 1.7 PbA 

There have been a number oT studies oT blood lead in populations living near 

smelters. The particle size is generally larger near smelters than in other urban 

conditions, and also the Tallout oT lead dust may be particularly heavy. 

In the study oT Yankel et al. (1977), the Tollowing variables were studied: 

1. Ambient air lead concentration. 

2. Lead concentration oT the soil. 

3. Age or the child. 

4. Cleanliness or the home. 

5. The occupation oT the parent. 

It was Tound that PbA (ranging up to 17 ug/m ) and lead in surTace soil (up to 

7500 ppm) were the most signiTicant Tactors. Table, 10.12, based on multivariate 

regression analysis, shows predicted PbB oT the children as a function of PbA and 

soil lead. For all levels of soil lead, the increase of PbB with PbA is approximately equivalent to a = 1. There is little difTerence between values Tor soil 

lead 500 and 1000 ppm, but at 5000 ppm the PbB levels are higher. The table is oT 

interest since lead in roadside dust in urban areas is typically or order 1000 ppm 

(Archer and Barratt, 1976b, Day et al. 1975). 

10.6 Blood lead versus water lead 

A number or studies have been nrade oT the relation between lead in blood and 

lead in water. A dirriculty is that the lead content oT the Tlrst. sample of wa«.«*i 

drawn Trom a tap in the morning is oTten much higher than that. oT water drawn filter 

flushing, owing to contact with lead plumbing overnight. 

-121-
In a study in Glasgow, where the water is soTt and lead pipework, common, 

Moore (1977) Tound a regression for blood lead versus lead in running samples of 

water 

PbB = 0.8 + 0.2 PbW 

where PbB and PbW are in u moles per litre . If PbB is in ug/100 g, PbW in Mg/1, 

the regression becomes 

PbB = 16+0.02 PbW 

In a later paper (Moore et al. 1977), the Glasgow data were re-examined statistically 

and a curvilinear relation between blood lead and first flush water lead was obtained. 

This suggests a non-linear relation between intake and blood lead, with a less 

steep increase in PbB when first-draw water lead exceeds about 1 umol/1 (200 ug/l), 

De Graeve et al. (1975) found an average PbB of 25.6 ug/100 g in 294 persons 

living in Gileppe, Belgium, in houses with soft water and lead pipes. In a control 

area, with hard water and pipes of other materials, the mean PbB of 261 subjects was 

12.7 Ug/100 g. From data given by Heusghem and de Graeve (1973), it appears that 

PbW (daytime samples) was 1040 and 20 ug/l Tor the two populations. Thus these 

observations would be consistent with 

PbB = 13 + 0.013 PbW. 

Moore took the average dally adult intake oT water to be 2 1. From ICRP (1975) 

data this is probably an overestimate, although it is very diTTicult to be certain 

oT the contribution oT water used in cooking. Windle Taylor (1971) found that the 

average amount of water taken as drinking water or in beverages made up from tap 

water (39 men and 8 women) was 1.26 1. Using this figure, Moore's regression 

implies that addition of 100 ug Pb orally in water increases PbB by 1.6 ug/100 g. 

However the later paper of Moore et al. (1977) seems to imply a larger effect, with 

100 ug/d orally increasing PbB by about 5 ug/l00 g. In Table 10.13, these results 

are compared with estimates derived from the experimental Pb dosing experiments of 

Kehoe, Stuik and Zielhuis, and Rabinowitz et al. in terms of the increase in blood 

lead (APbB) in relation to the extra oral lead (Al). Also given is a theoretical 

estimate based on fractional uptake from the gut, f = 0.15, fraction of uptake from 

© 

gut attached to red cells, f b = 0.55, and biological half-life in blood T^ = 18 d. 

Stuik and Zeilhuis gave their subjects oral doses of Pb for 21 days only, and 

the APbB/AI figure derived from their results should be increased to about 3 to 

correspond to a quasl-equilibrium situation. 

In Table 10.14 for comparison the ratio PbB/I of total blood lead to totnl oral 

intake, according to various authors, is summarised. The estimates of I are based 

on surveys of lead in diet, or lead in feces, and do not allow for uptake in the 

lungs of Pb in ambient air or in cigarettes. There is also some doubt whether 

dietary studies can be sufficiently exhaustive to Include every source of oral 

Intake. The ratio PbB/1 in the USA studies oT Kehoe, GriTTin et al. , and Tepper 

and Levin appears higher than that oT the European studies or Nordman (1975) and 

-122-
P.25 

Zurlo and GriTrini (1074). 'g'his may partly reTlect lower dietary lead and a higher 

proportional contr''-,:»'Lion of inhaled lead (ambient and cigarette) in the USA. 

10.7 Lead in chilG: ••;;-.:s biuoti 

Children have a higher metabolic rate than adults, and they inhale more air 

and eat more Tood, per unit body weight. Barltrop (1972) culoulated that a 2 ymr 

old child, whose body weight was 18$ oT that or an adult, ingests 50$ as much lead 

in diet, and inhales 40$ as much lead in air as an adult. IT the Tractional 

retention in the lung (T ), and Tractional uptake Trom the gut (f ) , are the same 

a g 

in adults and children, then, on Barltrop's figures, the 2 year old child's uptake 

or lead per unit body weight would be 2 to 3 times that or an adult. For a 10 year 

old child, the Tactors are as shown in Table 10.15. 

Moreover, there is evidence that both f and f. may be greater in children 

than in adults. The retention or aerosols in the lung depends on the dimensions 

oT the airways passages. Taking this into account, James (1978) has calculated 

the uptake oT particulates by inhalation by a 10 year old to be 1.6 to 2.7 times 

that or a man per unit body weight, depending on the particle siz e and level or 

physical activity. For child/woman, the ratios are 1.1 to 1.3. 

HoA-ever, several surveys oT blood lead in children and their mothers 

(Table 10.16) show ratios child/mother oT 1.2 to 1.4, which is about the same as the 

ratio or air intakes and rather less than that oT Tood intakes (Table 10.15). As 

the PbB ratio in adult man/woman is also about 1.3 (Goldsmith and Hexter, 1967, 

Tepper and Levin, 1975, Flindt et al. 1976), i t appears that there is littl e 

diTTerence in PbB in children and adult males under similar environmental conditions. 

Presumably, iT the Tractional retention in the lung, and the Tractional uptake Trom 

the gut are higher in children than in adults, these Tactors are balanced by more 

rapid turn-over or lead in the child's body. This conclusion may not be valid in 

heavily contaminated areas near lead smelters, where Tallout oT lead and high levels 

in dust contribute another mode oT entry. 

10.8 Resorption oT lead Trom bone 

One or the most diTTicult aspects oT predicting long term relationships or 

lead in blood to lead inhaled or ingested is the resorption and re-entry into blood 

oT lead stored in bone. Since the time scale over which this occurs is oT order 

years, only very long term experiments are directly relevant, though indirect estimates can be made by various means. The evidence Tor and against a signiTicant 

contribution oT bone lead to blood lead may be summarised as follows: 

(a) Kehoe's experiments 

After the conclusion of the periods of daily oral ingestion or lead, 

Kehoe (196lb) maintained measurements oT the lead balance oT three subjects 

Tor periods oT 896 (EB), 280 (MR) and 168 (IF) days. From Fig. 11 oT Kehoe's 

paper, which gives the accumulative lead balance, i t can be deduced that the 

stored lead was eliminated with apparent decay constants X oT about 0.3 , 0.08 

and 0.6 yr~ respectively. Kehoe noted the discrepancy Iwt.wfen thf rrs»ili.«i 

-123-
with MR, who eliminated only about 8$ or his stored lead in 10 lunar months, 

and EB, who eliminated halT in 23 months. Kehoe does not give inTormation 

to show whether the resorption Trom bone was reTlected in PbB levels, but IT 

the fraction oT the elimination that took place in urine, and the renal 

clearance, were normal, then a substantial contribution to PbB would be 

expected. 

(b) Bone lead versus age 

Barry (1975) Tound that lead in the skeleton oT non-occupationally 

exposed persons increased with age. However, the rate oT increase (Fig. 10.6) 

corresponds to a long term storage oT about 9 ug/d. The average uptake or 

lead Trom the gut in the UK is probably about 40 ug/d. IT about halT oT this 

goes to storage, then a substantial part, but probably not all, oT the storage 

may be Tor liTe. 

(c) Blood lead versus age 

Barry (1975) Tound no signiTicant eTTect oT age on Pb in blood or soTt 

tissue at post mortem, and Tepper and Levin (1975) Tound no signiTicant 

regression oT PbB on age in a survey oT 1127 non-smoking women in the USA. 

De Graeve e t al. (1975) in Belgium, Tound no signiTicant eTTect oT age on PbB 

in a control population, but in a population (136 men, 81 women) exposed to 

high levels oT Pb in drinking water, there was a signiTicant increase in PbB 

from 20 ug/100 g at age 20 to 31 ug/100 g at age 61-65 for men and 9 Ug/100 g 

at age 20 to 23 Mg/100 g at age 61-65 for women. 

It is possible that any efTect or resorbed Pb Trom bone on PbB in an 

ageing population may be balanced by a lower oral and respiratory intake, due 

to lessened activity . 

(d) Blood lead in occupational versus non-occupational groups 

It is commonly reported that enhanced PbB persists in highly exposed 

occupational workers long after their exposure has ended. Barry (1975), 

found mean skeletal, soft tissue and blood lead in non-occupational and former 

occupational subjects at post mortem as shown in Table 10.17. The difference 

in the PbB value of the two groups is oT doubtful significance, but i f i t is 

accepted and ascribed to resorbed bone lead, then a simple pro-rata calculation indicates that very approximately a quarter of Pbfc in 6 noma! adult <TOV 

be derived from skeletal lead. 

(e) Isotopic ratios in lead and blood 

Manton (1973) measured the relative abundance of the stable lead Isotopes 

Pb, Pb and ^°Pb in the blood or two South Africans who had lived in 

Dallas, Texas Tor 8 and 5.5 years and also in the blood oT their American-born 

wives. DirTerences were ascribed to resorption oT lead Trom bone which had 

been laid down in South ATrica where the isotopic ratios in diet diTTer Trom 

those in the USA. In a further paper (Manton, 1977), this analysis has been 

refined to show that 4 to 8$ of a subject's PbB is skeletal in origin during 

-124-
P.27 

the late summer, but 23 to 25$ in winter. The sensonal variation i* at*rrlhrd 

to variations in vitamin D. 

204, 

204 (T) UCLA experiments with Pb 

As previously discussed in Section 10.4, the 'plateau' levels of ""'Pb in 

blood showed that only about half the total PbB could be ascribed to current 

dietary lead. Unless there were unidentiTied sources, the remainder is 

attributable to skeletal lead and Inhaled lead. An analysis oT the likely 

input Trom airborne lead (PbA = 2 ug/m ), suggests that this might account 

Tor 25 to 30$, leaving 20 to 25$ or PbB ascribed to resorbed bone lead. 

The conclusions are bound to be uncertain, and i t is not easy to envisage 

experiments or surveys which would make them more certain. IT 25$ oT PbB in an 

adult is ascribed to skeletal lead, and 75$ to current dietary and respiratoryuptake, then a factor 100/75 = 1.3 should be applied to a (as estimated Trom 

experiments lasting up to several hundred days) to allow Tor the eventual re-entry 

into blood or lead which is transTerred to storage initially . 

10.9 Possible scheme or uptake and excretion oT lead 

As mentioned in the introduction, the ideal object would be to understand the 

contribution oT all the various sources or lead to PbB. In Table 10.18 a possible 

scheme or such a balance sheet is given, Tor an adult male resident oT a large city 

in the U.K. PbA has been taken as 1 ug/m , which is near the upper limit or annual 

means reported rrom the central areas oT citie s such as Birmingham (Archer and 

Barratt, 1976a), Bristol (Day e t al. 1977) and London (Lawther et al. 1973), excluding the immediate vicinity oT major roads. The amount oT ai r breathed has been 

taken as 15 m /d, and deposition in lung as 50$. 

The uptake rrom rood and drink has been taken as 41 ug/d (t5$ absorption 

in the gut) as compared with 30 ug/d (10$ absorption) which is commonly taken 

(e.g. Barltrop, 1972). As mentioned previously, the 10$ absorption oTten quoted 

seems to be based largely on comparisons or urinary and dietary lead, with no 

allowance Tor endogenous Tecal excretion. The Harwell rinding oT F A' = 0.5, is 

oT considerable importance in drawing up balances. 

The PbB level or 22 ug/100 g in Table 10.18 is that Tound in adult nonoccupational ly exposed males in Manchester. A similar level has been reported 

from Birmingham (DOE, 1978). The urinary excretion is 24 ug/d, from Thompson's 

(1971) measurements on 5 Manchester males. The renal clearance is thus 100/22 = 

4.5 g/hr (compare Table 10.9). With FgAJ = 0.5, endogenous fecal excretion is 

12 Mg/d, and there is a net positive balance or 12 Ug/d. Barry (1975) Tound 

an accumulation oT skeletal lead equivalent to 9 ug/d (Fig. 10.6). In the 

example or Table 10.18, PbA contributes 7.5 ug/d to uptake or lead, whereas rood 

and drink contribute 41 ug/d. In the USA, where PbA may be higher in NOTM: »-l»l#-s 

-125-
P.28 

anU tht lead content of food is lower according to some authors, the proportionate 

contribution oT PbA may be higher. It will also be higher in restricted zones 

. 3 

alongside motorways and busy urban roads in the U.K., where PbA exceeds 1 ug/m 

(Section 3.5 above). 

A table similar to Table 10.18 could be drawn up Tor a man who drinks 1.2C. l/d 

OT water with lead content 100 ug/l, in addition to the normal dietary intake. 

Assuming 15J( uptake Trom the gut, the contribution from water is 19 ug/d. Assuming 

other intakes as in Table 10.18, the total intake is then 48 • 19 = 67 ug/d. If 

the relationship between uptake and PbB is linear then PbB would be increased to 

23 x 67/48 = 32 ug/100 g. Thus an increased intake of 126 ug/d gives an increased 

PbB of 9 ug/100 g. In the notation of Table 10.13, APbB/Al = 7 ug/ioo g per 

100 ug/d. This is about twice as great an increase as appears from experimental 

studies. Probably the explanation lie s in a non-linear relation between Intake of 

lead and PbB (Moore e t al. 1977). 

It is possible that there are.significant sources of uptake not accounted Tor. 

Two possibilitie s are lead in cigarettes and lead in house dirt. Comparisons oT 

PbB in smokers and non-smokers have been inconclusive. Tepper and Levin (1975), 

with women subjects, Tound PbB = 17.3 ug/100 g Tor smokers compared with 

15.8 Ug/100 g Tor non-smokers. A contribution Trom ingestion oT dust is even more 

diTTicult to assess. IT i t is important, i t should aTTect children more than 

adults, and the comparison oT PbB in children and their mothers (Section 10.7) does 

not suggest a very large factor. 

A value oT a can be deduced Trom Table 10.18 with the proviso that a so deduced 

reTers not to the eTTect on PbB oT an additional intake or lead Trom PbA but rather 

to the contribution oT PbA to the total PbB. By proportion: 

Total uptake oT Pb = 48 ug/d 

Uptake Trom air = 7.5 ug/d (PbA = 1 Ug/m3) 

Total PbB = 22 ug/100 g 

7.5 x 22 _ - A a = —55 3.4 

Calculated in this way, a includes the contribution from lead which is transferred to storage in bone but subsequently resorbed, as it refers to a long term 

balance. For comparison, the value of a obtained from the Pb work (2.0 ug/100 g 

per ug/m if deposition in lung is 50$) should be increased by whatever factor is 

deduced from the data on resorption of stored Pb referred to in Section 10.8. If 

this factor is 1.3, then a (long-term) becomes 2.0 x 1.3 = 2.6. 

(1) Griffin et al. (1975), and Bogen et al. (1976) both found daily intake of 100 to 120 

Ug/d. Both studies were from the Eastern States. Kehoe (196la) found a mean 

230 ug/d by analysing the food and beverages of 10 oT his associates in Cincinnati. 

However Rabinowitz (1974) in Los Angeles Tound a normal diet to contain 365 Ug/d, 

and two specially selected low lead diets (2500 calories) contained 167 and 185 ug/d. 

He also Tound that the Pb content oT food as determined by his method (spiking with 

2°8Pb followed by mass spectrometry) gave higher results than methods used elsewhere, 

possibly owing to the dlfriculty oT ensuring complete dissolution or lead in Tood. 

Alexander et al. (1973) Tound an average oT 220 ug/d in the diets oT 4 children with 

body weight between 25 and 32 kg. 

-126-
P.29 

To compare with Table 10.18, Table 10.19 shows the typical components or lead 

uptake according to Ainsworth et al. (1977). These authors take the daily lead in 

Tood to be 143 Ug/d (MAFF, 1975) and the daily lead in water 40 ug/d (0.02 mg Pb/l, 

2 1/d intake). With 8$ and 10$ uptake Tram the gut oT lead in Tood and water 

respectively, Ainsworth et al. obtain a total dietary uptake oT 15.4 ug/d, which is 

only a third oT that calculated in Table 10.18. Assuming PbA = 1 Ug/m , and 35$ 

deposition in the lung, Ainsworth e t al. Tind that air lead contributes 25$ oT the 

total. On this analysis, iT PbB = 22 ug/100 g, and the various components contribute 

pro rata to PbB, then a = 5.5, which is larger than other methods oT calculation 

suggest. Also, the daily uptake oT 20.6 ug Trom gut and lung postulated by 

Ainsworth et al. compares with mean output in urine alone or normal subjects reported 

as 25 ug/d (Thompson, 1971), 30 ug/d (Kehoe, 196la) and 33 Mg/d (Rabinowitz et al. 

1977). Hence, i r the uptake is as small as 20.6 ug/d, both endogenous Tecal excretion and storage in bone must be negligibly small. There is probably more uncertainty 

about the daily uptake oT lead Trom Tood and water than the daily uptake Trom the 

atmosphere. 

10.10 Conclusions 

The various estimates or the Tactor a relating PbB to PbA are summarised in 

Table 10.20. As already discussed by MahaTTey (1977), there is a consensus oT 

experimental and epidemiological results giving a in the range 1 to 2 ug/100 g per 

Ug/m . However, iT instead oT the elevation oT PbB to be ascribed to PbA, the 

Tractional contribution or PbA compared with other sources oT lead in the diet is 

considered (as in Table 10.18), and the contributions to PbB taken pro rata, the 

value oT a appears higher. A similar discrepancy can be detected in studies or the 

eTTect on PbB oT lead in water. 

The only obvious explanations are either: 

(a) there are important unquantiTied sources oT intake or lead (Tor example, 

cigarettes and alcoholic drinks) 

or (b) the relation oT PbB to lead intake is non-linear, so that exposure to PbA 

does not increase PbB pro rata to the increased intake or lead. 

The same point is illustrated in Table 10.21. The Tirst row shows the ratio 

oT the intake oT lead Trom PbA to the intake Trom dietary sources according to the 

analysis oT Table 10.18. Thus Tor PbA = 1 ug/m , the ratio is 7.5/41 = 0.18 and Tor 

PbA = 2 or 5 ug/m the ratio is increased pro rata assuming a linear relationship. 

This estimate depends on the lead content or diet, and the Tractional uptake rrom the 

gut as well as on the uptake oT PbA in the lung. It is probable that the lead 

content or diet is decreasing with time (Ministry or Agriculture, Fisheries & Food, 

1975). IT PbA remains the same, its proportional contribution to total lead uptake 

is likely to increase. In the second row or Table 10.21, the ratio deduced by 

Rabinowitz et al. (1973) is given. For a subject in Los Angeles exposed to PbA = 

2 Mg/m these authors deduced 13 Ug/d uptake Trom air compared with S3 ug/d dietary, 

giving a ratio oT 0.39. The last two rows or Table 10.21 show the ratios d*dur t:<\ 

from straight line regressions of PbB on PbA from Tokyo and CaliTornia reTerred to in 

•127-
"' •" f ^L*^i»^*irn» .I T —p.-

P.30 

Section 10.5. The intercept or the regression on the PbA axis (i.e. the extrapolated 

value oT PbB when PbA = 0) is used to estimate the dietary contribution to PbB. Once 

more a linear relationship is assumed, and no Account has been taken oT the possible 

InTluence oT sociological and other factors related to residence. 

There is conQicting evidence as to whether the eTTect or PbA on PbB, or the 

proportion oT total intake attributed to PbA, is greater Tor children than for adults. 

The analysis oT Table 10.16 and Section 10.7 suggests little diTTerence, but the epidemiological studies in Tokyo and CaliTornia suggest a bigger eTTect in children, 

possibly connected with indirect uptake oT lead from other sources correlated with 

PbA. 

-128-
P.31 

TAIiLE 10.1 

Sioi-agc of U-aJ by Kehqc'd subjects rcccivim; Uaiiv oral Ufasu^ 

Subject 

Duration of dosing (d) 

Approximate dail y dose (mg) 

Total dose (mg) 

Pb i n food and drink (mg) 

Total ingested Pb (mg) 

Lead stored (mg) 

- as fraction oT ora l dose 

- as Traction or tota l ingested 

Duration or Tollow-up (d) 

Lead released Trom storage (mg) 

1 - as Traction oT stored Pb 

SW 

420 

0 . 3 

126 

88 

214 

12 

0.095 

0.056 

-

-

-

MR 

1456 

1 

1443 

528 

1971 

118 

0.083 

0.060 

280 

7 

0.06 

EB 

644 

2 

1287 

132 

1419 

110 

0.086 

0.078 

896 

68 

0.6 2 

IF 

122 

3 

336 

27* 

363 

55 

0.16 4 

0.152 

168 

15 

0.27 

* Keohe does not give IF's daily Pb in Tood and drink during the experimental period. 

The Tigure quoted is IF's daily Pb during a control period, a s given by Kehoe 

(1961a), Table 12. 

TABLE 10.2 

Uptake, excretion and storage of lead in Kehoe's subjects MR and EB 

Subject 

Duration (days) 

Lead ingested (ug/d) 

- in rood and drink 

- in solution 

- tota l (I) 

Lead eliminated (ug/d) 

- in Teces (F) 

- in urine (U) 

- tota l 

Lead stored (S) (ug/d) 

Assuming F AJ =0. 5 Tor both 

Endogenous Tecal lead 

Fe (Mg/d) 

Uptake Trom gut (ug/d) 

G = U + Fe + S 

Fractional uptake 

Tg = G/I 

Fraction oT uptake retained 

f

gs - Vfe 

Assuming FCAJ = 1 Tor EB. zer 

F

e 

G 

f

g 

f

g s 

MR 

Dosing 

1456 

363 

991 

1354 

1195 

78 

1273 

76 

subjects 

39 

191 

0.1 4 

0.4 0 

o Tor MR 

-

154 

0.11 

0.49 

Follow-up 

280 

329 

-

329 

298 

57 

355 

-26 

28 

59 

0.1 8 

^ 

31 

0.09 

Dosing 

684" 

194 

1881 

2075 

1807 

107 

1914 

161 

53 

321 

0.15 

0.5 0 

107 

375 

0%18 

0.43 

EB 

Follow-up 

684 

331 

-

331 

342 

80 

422 

- 9 0 

40 

30 

0.09 

80 

70 

0.21 

-129-
TABLE 10.3 

Lead balance in Kehoe's subject FC beTore, during and after 

exposure to airborne lead in an experimental chamber 

Length oT study (d) 

Lead ingested in Tood and drink 

Lead inhaled (A) 

(deposited in lung) 

Total 

Lead eliminated in feces (F) 

in urine (U) 

total 

Lead stored in body (S) 

Assuming FCAJ =0. 5 

Endogenous fecal lead (F ) 

Total uptake = U + Fg + S 

Uptake from gut=U+F e + S- A 

- as fraction of ingested (Ts) 

Retained lead as fraction of 

total uptake 

fs = S/(U + Ffi + S) 

Preliminary 

period 

532 

Total 

mg 

ISO 

130 

111 

12 

123 

7 

8.6 

25 

25 

ug/d 

244 

244 

209 

23 

232 

12 

11.5 

46.5 

46.5 

0.19 

Experimental 

period 

616 

Total 

mg 

134 

98 

232 

140 

45 

185 

47 

22.5 

114.5 

Ug/d 

217 

159 

376 

227 

73 

300 

76 

36.5 

185.5 

16.5 | 26.5 

0.12 

0.38 

Follow-up 

period 

532 

Total 

mg 

91 

91 

80 

14 

94 

- 3 

7 

19 

19 

Ug/d 

172 

172 

150 

27 

177 

-5 

135 

35.5 

35.5 

0.21 

TABLE 10.4 

204 Endogenous Tecal excretion oT Pb by UCLA subjects 

Subject 

A 

B 

C 

D 

Mean 

Days from 

start of 

experiment 

ISO 

150 

130 

140 

155 

171 

227 

110 

139 

Days from 

end of 

dosing 

26 

46 

6 

16 

31 

47 

103 

28 

57 

End. fecal 

excretion 

Ug/d 

1.8 

1.2 

2.6 

1.5 

1.2 

0.7 

0.05 

1.7 

1.0 

204Pb in 

blood 

Mg/g 

0.0265 

0.0118 

0.0394 

0.0299 

0.0205 

0.0131 

0.0025 

0.0282 

0.0160 

End.fecal 

g blood/d 

68 

102 

66 

50 

59 

53 

20 

60 

63 

60 

clearance 

g blood/h 

2.8 

4.3 

2.8 

2.1 

2.5 

2.2 

0.8 

2.5 

2.6 

2.5 

-130-
P.33 

TABLE 10.5 

204 Uptake and storage oT Pb in UCLA subjects given dally oral doses 

Subject 

Duration oT tracer intake (d) 

1 204 

Pb ingested (ug/d) 

204Pb eliminated (ug/d) 

- in feces 

- in urine (U) 

204Pb stored (S) (ug/d) 

- total (ug) 

Pb in bone at biopsy (Mg) 

Endogenous fecal excretion (Fg) (ug/d) 

Uptake from gut (Mg/d) G = U + Fg + S 

- as fraction of ingested (f ) 

Fraction oT uptake stored T = S/G 

gs | 

A 

104 

204 

188 

8.4 

8 

830 

702 

4.4 

20 

0.10 

°-4 

B 

124 . 

185 

174 

4.7 

6 

630 

674 

1.8 

13 

0.07 

0.5 

D 

83 

105 

94 

5.4 

5 

1.8 

13 

0.12 

0.4 

Notes 

(a) 

(a) 

(a) 

(b) 

(c) 

(a) 

(d) 

Notes: (a) Data oT Rabinowitz et al. (1976b) 

(b) The daily total Pb in urine was 0.41, 0.27 and 0.36 Mg Tor the 

subjects A, B, D. The isotopic ratios in blood and urine were 

identical at all times. The average daily 204pD ^ g calculated 

by multiplying the total PbU by the 204pb/total Pb ratio in blood. 

This last ratio was deduced Trom the

 204PbB and total PbB figures 

f

iven by Rabinowitz et al., averaged on the duration oT intake or 

04pb. 

(c) The bone biopsy on subject A was done on day 115, aTter the end 

or the dosing period, but on subject B on day 105, beTore the 

end oT dosing (Rabinowitz, 1974). The total storage oT

 204 Pb 

has been calculated up to the time oT biopsy. 

(d) F_ calculated from the endogenous Tecal excretion measured aTter 

the end oT dosing, assuming the rate both during and aTter 

dosing to be proportional to

 204PbB. 

TABLE 10.6 

2CV4 

Estimates oT halT-liTe oT Pb in blood oT UCLA subjects 

Subject 

Estimated blood mass 

T^ (days) by method (a) 

(b) 

(c) 

Analysis or Rabinowitz et al. 

(exchange rates oT Tirst pool) 

X"' (days) 

T^ (days) 

A 

4.9 

24 

18 

23 

34 

24 

B 

6.3 

28 

24 

30 

40 

28 

C 

6.3 

37 

26 

D 

4.6 

31 

36 

25 

40 

28 

E 

6.3 

18 

27 

19 

-131-
r TmjfT r^'Trrwr -r^-

TABLE 10.7 

204, Pb and total Pb in diet and blood oT UCLA subjects 

(Rabinowitz et al. 1976b) 

Subject 

204PbB at plateau (ug/l00 g) 

Total PbB (ug/100 g) 

Ratio

 204Pb/Pb in blood 

Oral dose oT

 204Pb (Mg/d) 

Dietary Pb (Mg/d) 

Total ingested Pb (Mg/d) 

204 Ratio Pb/Tb ingested 

Fraction or blood lead attributed 

to current diet 

A 

7.6 

25 

0.30 

204 

156 

360 

0.57 

0.53 

B 

4.8 

18 

0.27 

185 

179 

364 

0.51 

0.53 

D 

5.4 

20 

0.27 

105 

188 

2S3 

0.36 

0.75 

TABLE 10.8 

Inhaled lead Intake by three methods (Mg/d) 

(Rabinowitz et al. 1977) 

Subject 

Lead balance 

Blood labelling 

Response to Tiltered ai r 

A 

16 2 4 

17 * 5 

-

B 

1 9 : 3 

16 2 6 

16 1 3 

D 

12 2 6 

8 1 4 

9 1 3 

E 

7 1 6 

12 1 2 

-132-
TABLE 10.12 

Predicted mean childhood blood lead (Mft/lOO ml) 

Tor various air and soil lead concentrations near amelter 

(Yankel et al. 1977) 

Air , 

Ug Pb/m 

1 

2 

3 

4 

5 

Soil (ppm lead) 

500 

26.7 

27.8 

29.0 

30.2 

31.5 

1000 

27.0 

28.1 

29.3 

30.5 

31.8 

5000 

29.3 

30.5 

31.8 

33.1 

34.5 

TABLE 10.13 

Elevation or blood lead Trom oral intake oT lead 

Author and subjects 

Kehoe (1961) 

SW 

MR 

EB 

Stuik & Zielhuis 

(1975) 

5 males 

5 Temales 

Rabinowitz (1974) 

Rabinowitz et al. 

(1976b) 

Preliminary subject 

Subject A 

B 

D 

Moore 1977 

Moore et al. 1977 

Theoretical, assuming 

Period or 

experiment 

(days) 

420 

364 

644 

21 

21 

45 

104 

124 

84 

Derived Trom 

assuming tap 

it 

r = o.is, r . 

g gt 

Pb (Mg/d) 

given 

orally 

300 

1000 

2000 

1400 

1200 

75 

204 

185 

105 

regression o 

water intake 

II u 

3 = 0.5, Dj = 

PbB (Mg/100 g) 

BeTore 

32 

30 

39 

20 

12 

ATter 

37 

55 

68 

42 

30 

<

204PbB) 

Nil 

Nil 

Nil 

Nil 

1.7 

7.4 

4.7 

4.5 

T PbB on PbW 

or 1.26 1/day 

II 

18 d 

Increase in PbB 

ug/100 g per 

100 Mg/d) 

(APbB/AI) 

1.7 

2.5 

1.4 

1.6 

1.5 

2.3 

3.6 

2.5 

4.3 

1.6 

- 5 

3.6 

-135-
P.36 

TABLE 10.14 

Blood lead and dietary lead 

(food and drink) 

Sex 

F 

M 

M 

M 

F 

M 

Oral intake 

I 

(Mg/d) 

124 

113 

230 

230 

180 

505 

PbB 

(Mg/100 g) 

16.2 

19.0 

26 

12.3 

7.9 

32.9 

PbB/I 

(Mg/100 g per 100 ug/d) 

13 

17 

12 

5.4 

4.4 

6.5 

References 

Tepper & Levin (1975) 

Griffin e t al. (1975) 

Kehoe (1961) 

Nordman (1975) 

Nordman (1975) 

Zurlo & GrifTini (1974) 

TABLE 10.15 

Ratio oT intakes oT air and Tood per unit blood volume 

for 10 year old children and adults 

(data from ICRP, 1975) 

Air (resting) 

Air (light activity) 

Food 

Child 

Man 

1.58 

1.61 

1.65 

Child 

Woman 

1.49 

1.27 

1.77 

Woman 

Man 

1.07 

1.27 

0.93 

-136-
P.37 

TABLE 10.16 

Lead in blood oT children and mothers 

(number or subjects given in brackets) 

Location 

Matlock & Buxton 

Derbyshire 

villages 

E. London 

Bristol 

N. Wales 

(copper pipes) 

N. Wales 

(lead pipes) 

Age oT 

children 

2-3 

2-3 

Pre-school 

Under 10 ( 1 ) 

Under 16 

Under 16 

PbB 

Children 

23.2 

(180) 

23.2 

(82) 

33 

(144) 

16.2 

(64) 

19.2 

(19) 

41.6 

(38) 

(Ug/100 ml) 

Mothers 

19.1 

(175) 

16.1 

(74) 

27 

(107) 

13.5 

(24) 

13.9 

(19) 

39.5 

(38) 

Ratio 

1.2 

1.4 

1.2 

1.2 

1.4 

1.1 

ReTerences 

Barltrop e t al. (19 74) 

Barltrop et al. (1975) 

Lansdown et al. (1974) 

Day e t al. (1977) 

Elwood et al. (1978) 

Elwood et al. (1978) 

(1) Children were grouped in age ranges 0-5 and 5-10. PbB was not 

signiTicantly diTTerent in the two groups. 

TABLE 10.17 

Lead in tissues at post mortem (Barry. 1975) 

Subjects 

Occupational 

Non-occupa tional 

Pb (mg) in 

bone 

507 

155 

soTt tissue 

14 

9 

Pbin^{o2§ 8 ) 

Mean 

31 

20 

S.E. 

6 

2 

-137-
TABLE 10.18 

Scheme of uptake and excretion oT lead by adult male 

in urban distric t oT U.K. 

P.38 

-'—'Ty'—W||» -

Uptake 

Intake in food and 

Fraction absorbed 

Uptake Trom gut 

Uptake from lung 

Total uptake 

Excretion 

Blood lead 

Urinary excretion 

Endogeneous Tecal 

Total excretion 

Storage 

drink 

in gut 

excretion 

270 Mg/d 

0.15 

41 Ug/d 

7.5 Mg/d 

48 Mg/d 

22 Mg/100 g 

24 Mg/d 

12 Mg/d 

36 Mg/d 

12 Mg/d 

Re Terences and Notes 

Thompson (1971) 

See Tables 2, 3, 5 

PbA = 1 Ug/m3 

ra =0. 5 

Flindt et al. (1976) 

Thompson (1971) 

Assuming F Aj = 0.5 

Compare Fig. 10.6 

TABLE 10.19 

Relative contributions to uptake oT lead in 

analysis or Ainsworth et al. (19773" 

Intake Mg/d 

Food 143 

Water 40 

Air 15 

Percentage 

uptake 

8$ 

10$ 

35$ 

Total 

Mg/d 

11.4 

4.0 

5.2 

Uptake 

$ oT total 

55$ 

19* 

25$ 

20.6 

-138-
P.39 

TABLE 10.20 

Summary or estimates oT elevation oT blood lead oT adults Tram 

exposure to air lead 

Method 

203 Pb 

203; Pb 

203 Pb 

Exposure oT subjects 

to PbA 

I I it <i 

Epidemiological 

ug/100 g per MgAi" 

j From estimates or uptake i 

j and excretion j 

i L 

1.1 

2.0 

2.6 

1.2 

1.6 

2.4 

0.8 

3.4 

Rererences and Notes 

Chamberlain et al. (1975), with Tfi = 

0.35, Tab = 0.5, T,^ = 16 d. 

Revised estimate with Tfi = 0.5, Tafc = 

0.55, Ti^ = 18 d. 

As above, if an additional factor 

1.3 for long term resorption of bone 

is assumed. 

Kehoe (1961b, 1966) (see Table 10.9) 

GriTTin et al. (1975) (see tables 10,9 

and 10.10). 

Tsuchiya e t al. (1975) - see Fig. 10.5 

assuming all variation in PbB can be 

ascribed to PbA, but note authors' 

comment at root of p.120. 

Johnson et al. (1975) (see Table 10.11). 

Section 10.9 above and Table 10.18. 

TABLE 10.21 

Summary oT estimates oT ratio oT contributions oT air lead to 

other lead intakes (adultsT 

Method 

As in Table 18 

204 

Pb (Rabinowitz et al. 1973) 

(Los Angeles) 

PbB/PbA regression oT Tsuchiya et al. 

(1975) - see Section 10.5 (Tokyo) 

PbB/PbA in CaliTomia (Johnson et al. 

1977) - see Section 10.5. 

PbA/other at PbA levels oT 

1 Mg/m 

0.18 

0.20 

0.15 

0.08 

/ 3 

2 Mg/to 

0.36 

0.39 

0.29 

0.16 

5 ug/m 

0.9 

1.0 

0.73 

0.4 

139-
P.40 

o 

o 

Ot 

St 

O 

O 

0_ 

o 

CM 

50 100 150 

Time from start of daily dose (days) 

A.E.R.E.R9198. FIG.10.1.

 20 *Pb IN BLOOD OF UCLA SUBJECTS (RABINOWITZ, 

et al.1976b) CURVES ARE FITTED BY METHOOIc) OF SECTION 10.3. 

-140-
*-TT*HWWP.41 

a. 

J I I I I I ' ' i I i 

T—i—i— r 

I I I I I X 

100 200 300 

Time (days) 

A.E.R.E.R9198. FIG.10.2. LOSS OF

 20 *Pb FROM BLOOD OF FOUR SUBJECTS 

AFTER WITHDRAWAL OF ISOTOPE FROM DIET (RABINOWITZ 

et al.1976b). 

-141 -
P.42 

"-**nr - ""• 

2 

UJ 

1 1 

The 

the 

——t 1——j 1 , 1 1 rnumbers neor the points ore 

numbers of subjects Bs16 0(1-exp-00245t l 

B= 5 3(1-exp- 0 0266t) 

Days 

A.E.R.E.R9198. FIG. 103. BLOOD LEAD OF DANNEMORA SUBJECTS EXPOSED 

TO MEAN 24-HOUR AIR CONCENTRATIONS OF 10 4f/g/m3 (ABOVE) OR 

3 1/ig/ m3 ( BEL OW ) . 

-142-
P.43 

Days 

A.E.R.E.R9198. FIG.10.4. INCREASE OF PbB IN TOLA et al's 

SUBJECTS ON BEGINNING WORK IN THE LEAD INDUSTRY. 

-143-
P.44 

"TWS-l'-^HJ^-rww--

2 0 -

E 

o 

o 

Ot 

"O 

O 

Or 

- 10 

*o 

o 

o 

m 

1 

. 

—. 

-

• 

0 

-

-

-

-

-

-

— 

• 

" 

• 

-

• 

-

-

-

L_ 

i 

^O*-' 

i 

i 

i 

1 

e 

i 

1 

o 

A 

A 

1 

i 

_ i _ 

—i r— 

o 

00000-'O** 

—J_.-J — 

i 

i 

1 

0 

o 

1 

• 1 

__!_ 

T " 

- -«-

•—1 — 

O 

..JU 

T ~ 

J 

—T— 

A 

A 

1 

1 

• 

— 

-

• 

" 

• 

-

-

-

-

-

— 

-

* 

-

-

* 

-

-

-

* , 

0 5 10 1 5 

Air lead (//g/m3) 

A.E.R.ER9198. FIG.10.5.PbA AND PbB IN TOKYO. 

Q POLICEMEN (TSUCHIYA et al.1975. FIG. 18) A MALE CHILDREN 

A FEMALE CHILDREN (TSUCHIYA et ol. 1977. TABLE 3). 

-144 -
E.R.E.R9198. F1G.10.6. LEAD IN 

DEATH.NORMALISED TO 70kg BODY 

100 

SKELETON AT 

WEIGHT 

-14S. 
Acknowledgements 

Thanks are due to the volunteer subjects Messrs. D.H.F. Atkins, K.F. Bi9hop, R.H. Hounam 

and Dr. A.N.B. Stott. Dr. Stott also supervised the experiments medically. Messrs. R.C. 

Fleming and M. Eagle helped with the experimental work, and Messrs. R.J. Evans and J.F. Smith 

took the blood samples. Dr. M. Inskip and Mr. M. J. Duggan provided racilities Tor air 

sampling at Chelsea College and County Hall respectively. Mrs. M. J. Cann provided inTormation and Miss J. Fenn secretarial services. 

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