Vol. 2 1 , No. 4 Printed in Great Britain

International Journal of Epidemiology © International Epidemiological Association 1992

Nonoccupational Determinants of Blood Lead Concentrations in a General Population HANS-WERNER HENSE,* BIRGIT FILJPIAK,* LADISLAV NOVAKt AND MARKUS STOEPPLERt

factors other than atmospheric lead were suspected to be significant sources of blood lead.6 Even low levels of PbB are considered hazardous and are of great public health concern.7 Recent evidence from epidemiological studies points to the potentially long-lasting effects of in utero exposure on neurobehavioural and cognitive development of children.8 Blood lead levels in maternal blood in these studies were as low as 100 u.g/l.9>10 Surveys of the adult general population with mean PbB levels around 150 ug/1 observed positive associations between PbB and blood pressure""16 or left ventricular hypertrophy17 over the entire range of PbB. It is of interest that a recent expert meeting postulated that such effects in adults may even be restricted specifically to low levels of PbB and that they were likely to disappear at higher blood lead concentrations.18 As a consequence, definitions of critical limits for PbB levels have been

Over the past two decades most industrialized countries have experienced significant decreases in atmospheric lead contamination. This has been predominantly attributable to legislative action which has enforced the widespread use of lead-free gasoline, and reduced certain canning and printing materials. The decreases in exposure to lead from inhalation and ingestion of food contaminated by atmospheric lead deposition were reflected in falls of mean blood lead (PbB) levels observed in several population studies.1"5 However, some investigations reported sizable declines in PbB levels (by 30-40100 ji*/l (%)

407 418 453 425 1703

85.3 91.3 93.2 90.1 90.1

31.1 32.4 39.2 39.4 35.9

57 59 58 56 57

79 84 85 83 83

119 133 132 126 128

23.1 32.8 31.8 27.8 29.0

380 443 447 391 1661

60.3 63.4 68.9 67.7 65.2

22.7 26.4 31.0 23.0 26.4

38 38 41 43 40

57 58 64 63 60

84 94 100 96 94

3.9 7.7 10.1 8.4 7.6

Men

Women 28-37 38-47 48-57 58-67 Total

TABLE 2 Pearson's correlation coefficients for the linear association of blood lead (PbB) (\ig/l) and log-transformed, In(PbB) with potential determinants. Men and women of the first follow-up examination of the MONICA Augsburg cohort study 1987-1988

Correlation coefficients ln(PbB)

PbB Determinant

Men

Age (years)

0.06* 2

Women

Men

Women

0.11"*

0.05ffl

0.14"'

ra

-0.03" 1

Body mass index (kg/m )

0.08"

Haematocrit (Vt)

0.17"*

0.24"»

0.17*"

0.25*"

Cigarettes smoked (No./day)

0.11*"

0.21"*

0.12"*

0.19*"

Alcohol consumption (g/day)

0.24"»

0.33"*

0.27"'

0.34*"

Alcohol consumption (beer) (g/day)

0.18"'

0.15*"

0.21"*

0.18*"

Alcohol consumption (wine) (g/day)

0.18*"

0.30*"

0.18*"

0.29*"

•P40 g/day

8.94

(3.19-25.11)

Determinant

DISCUSSION We investigated nonoccupational determinants of blood lead concentrations in participants of a population-based cohort study. Although the original sampling procedure and the selective participation raise questions concerning the representativeness of the subjects, it can be inferred from the data, that the Augsburg study population at large was exposed to low levels of lead. The average lead burden was considerably lower than that reported for populations from different countries in the late 1970s and 1980s31"35 but it compares very well with recent data from a national survey conducted in Germany in 1985-1986 where median PbB was 79 u.g/1 in men and 60 u.g/1 in women.36 This result may reflect actual reductions in exposure as well as improved ultratrace analytical techniques with high accuracy.27'28 The extraordinarily laborious analytical approach adopted in our study will in addition have significantly increased the reliability of individual PbB determinations and hence the discriminative power of the statistical calculations. Age had some influence on PbB levels and was greater for women notwithstanding the consistently higher blood lead levels in men. Adjustment for the available anthropometric and lifestyle variables by a multiple regression model fitted jointly for males and females reduced the crude overall mean PbB difference of 24.9 ug/1 by only about 30% and a residual difference of 17.8 ug/1 PbB (95% CI: 15.4-20.2) between men and women remained unexplained. It is most likely that gender-related factors other than lead exposure in the workplace are involved in creating this difference.37'38 A prominent feature of our study is the finding that PbB levels in a low-exposure population are strongly determined by individual characteristics such as the haematocrit and lifestyle variables like alcohol consumption and, to a lesser extent, cigarette smoking. It is interesting to note that haematocrit (or red blood cell count, haemoglobin) was found in a number of population studies to be strongly and positively related to PbB concentrations6"39 but that the impact of this association is hardly ever addressed.'40 We assume that the relationship reflects primarily the lead-binding capacity of blood because more than 95% of lead is bound to haemoglobin and the membranes of the erythrocytes.41 This contention is supported by the finding that the shape of the fitted curves for men and women in Figure 1 are practically identical once the absolute gender difference of 4% in haematocrit values is taken into account, i.e. after shifting the curve for males by this amount to the left. Using the assumption that the statistical haematocrit-PbB association indeed reflects binding capacity this similarity can be ex-

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Age (yean) 38-47 48-57 58-67 Haematocrit Cft-42) Haematocrit 2 Place of residence (rural •= 1) Body mass index (kg/m 2 ) Cigarettes smoked (No./day) Alcohol consumption—beer (10 g/day) [Beer]J (10 2 g/day) Alcohol consumption—wine (10 g/day) [Wine]2 (102 g/day)

P

Women

757

758

INTERNATIONAL JOURNAL OF EPIDEMIOLOGY

120

38

40

42

44

46

48

50

52

54

Hematocrit [%] FlOURE 1 Crude mean blood lead (\ig/l) with 95 % confidence intervals in seven categories of haematocrit and fitted regression line over the gender-specifk ranges of haematocrit values. Participants from the first follow-up examination of the MONICA Augsburg cohort study 1987-1988.

plained theoretically because men and women do not normally differ in their mean haemoglobin content per erythrocyte.42 As discussed above the absolute PbB levels for a given adjusted haematocrit still remain higher in men than in women perhaps as a consequence of additional factors regulating lead metabolism differentially in the sexes.38 The observed positive relationship between PbB levels and haematocrit in our study is not at variance

with the well-known observation of the suppressive effects of toxic PbB levels on the haematopoietic system.43 The threshold for such effects is, however, considerably higher (approximately 250 ng/1)43 than the levels found in the general population. In the latter, the normal range of haematocrit values translates into PbB increases of lS-lO'fa. Therefore, haematocrit is a determinant of PbB which may operate as a, yet unrecognized, confounding or modifying variable in

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36

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120

120

110

100

o>

90

J lead

3.

ca

80

70

60 •

MEN

I n

5 > D

M

o

Z CD

O WOMEN 50

0

10

20

30

40

50

60

70

80

Alcohol consumption |g/day] by beer

90

100 110

0

10

20

30

40

50

60

70

80

90

100 110

Alcohol consumption (y/tlayj by wine

FlOURE 2 Crude mean blood lead (\ig/l) with 95 W confidence Intervals in categories of alcohol consumption by beer (left panel) and wine (right panel) and fitted regression line over the gender-spec(fic ranges of alcohol consumption. Participants from the first follow-up examination of the MONICA Augsburg cohort study 1987-1988.

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INTERNATIONAL JOURNAL OF EPIDEMIOLOGY

Cigarette smoking is linearly and only moderately associated with PbB levels in males but the association is somewhat stronger in females. Differences over the range of consumption found in our study subjects show clearly that the relative impact of drinking beer and wine is much greater than that of smoking. This confirms results from other population studies.35-3*44^ Smoking habits at the sex-specific 90th percentile value of our study participants' distribution were associated with PbB levels 6% higher in men and 9% higher in women relative to nonsmoking subjects. This contrasted with PbB concentrations raised by 18% in men and 16% in women relative to abstainers when beer consumption, and by 13% and 26%, respectively, when wine consumption, reached an amount equivalent to the sex-specific 90th population per cen tiles. We evaluated, for the Augsburg population, the impact of smoking and total alcohol consumption on the

probability of women of childbearing age having PbB levels above 100 ug/1, a threshold presently considered hazardous to the health of the fetus.7i8>49 In this group of younger women, smoking and drinking were much more prevalent than at older ages and hence the risk association was stronger than in the analyses involving women of all ages. Smoking significantly increased the odds of having PbB levels ^100 ug/1 by a factor of 2.5 and the odds ratio for heavy drinking was 8.9. In accordance with this estimate, the baseline assessment of mothers in the Boston Lead Study showed that mothers of children belonging to high and low cordblood lead groups were significantly different, apart from age, only in their smoking duration and alcohol consumption.9 These two habits appear to be the dominating determinants of PbB levels endangering the future mental development of infants. We conclude that an individual's haematocrit and the amount of cigarettes smoked and of alcohol consumed are relevant determinants of PbB levels in the general population. The as yet little recognized PbB influence of haematocrit may affect aetiological research at low lead levels. Current thinking assumes that the increase in blood lead levels brought about by smoking and alcohol consumption may contribute to diseases of the circulatory system and the kidney as well as to an impaired mental development of the offspring.50 The public health impacts of these findings in terms of further research and preventive action deserve greater attention. ACKNOWLEDGEMENT We gratefully acknowledge the support of Profs U Keil and E Ritz who initiated the present investigation. Kerstin Honig-Blum was most helpful in data handling and producing the figures. The study was financially supported by the Federal Ministry of Research and Technology grant No. 0706334 7. REFERENCES 1

2

3

4

5

6

Annest i L, Pirkle J L, Makuc D et at. Chronological trend in blood lead levels between 1976 and 1980. NewEnglJMed 1983; 3M: 1373-77. Hinton D, Coope P, Malpreu W A, Janus E D. Trends in blood lead levels in Christchurcb (NZ) and environs 1978-85. J Epidemiol Community Health 1986; « h 244-48. Elwood P C. Change* in blood lead concentrations in women in Wales 1972-1982. Br Med J 1983; 2*5: 1553-55. Elwood P C, Toothfll C. Further evidence of a faD in blood lead levels in Wales. J Epidemiol Community Health 1986; 40: 178-80. FJinder C O, Friberg L, Lind B et al. Decreased blood lead levels in residents of Stockholm for the period 1980-1984. Scand J Work Environ Health 1986; 12: 114-20. Arnetz B B, Nicolich M J. Modelling of environmental lead contributors to blood lead in humans. Int Arch Occup Environ Health 1990; 62: 397-402.

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aetiological research. For example, Grandjean recently indicated that adjustment for binding capacity On this case haemoglobin) in addition to other factors made the crude correlation between PbB and blood pressure completely disappear.39 Our study confirms the association between alcohol consumption and blood lead concentrations commented on in previous reports.33'44"47 The relationship was slightly stronger at lower levels of alcohol intake and it differed significantly by type of alcoholic beverage. The latter finding is not supported by results from the UK and Denmark44"46 where wine and beer drinking appeared not to be differentially related to PbB. However, most subjects in these studies drank beer only. The consumption patterns among our study subjects reflect a more varied intake of beer and wine with about one-third of participants consuming wine and 77% of men and 31% of women drinking beer every day. Conversion of average grams of alcohol consumed per day into volumes of beer and wine shows that equialcoholic intakes of, say, 40 g/day refer to one litre of beer but only 0.4 1 of wine. Based on average lead contents given for beer and wine samples available on the German market,48 namely 22 Hg Pb/1 beer and 101 ug Pb/1 wine, it can be calculated that the consumption of 40 g alcohol from beer is associated with an average daily lead supply of 20 ug whereas the same amount of alcohol ingested from wine supplies 40 ug Pb every day. The order of magnitude of this difference resembles very closely the one found in our regression analyses. We therefore suggest that most of the PbB rises found at moderate intakes of beer and wine originate from increased lead supply and not from metabolic disturbances as suspected by some investigators.43

N O N O C C U P A T 1 O N A L DETERMINANTS O F L E A D IN BLOOD 7

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Nonoccupational determinants of blood lead concentrations in a general population.

We investigated the influence of various nonoccupational factors on blood lead levels (PbB) in a sample from the general population of southern German...
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