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Grandjean et al. 

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Manuscript submitted to 

American Journal of Epidemiology 

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BLOOD LEAD-BLOOD PRESSURE RELATIONSHIPS: 

ALCOHOL INTAKE AND HEMOGLOBIN AS CONFOUNDERS 

P.Grandjean,1 H.Hollnagel,^ L.Hedegaard,^ 

J.M.Christensen^ and S.Larsen^ 
P.3 

Grandjean et al. page 2 

'Department of Environmental Medicine, Odense University, 

J.B.Winslowsvej 19, 5000 Odense, Denmark 

^The Population Studies in Glostrup, Copenhagen County 

Hospital, Glostrup, Denmark 

^Danish National Institute of Occupational Health, Copenhagen , Denmark 

Deceased 

Reprint requests to Dr. Philippe Grandjean, Department of 

Environmental Medicine, J.B.Winslows vej 19, 5000 Odense C, 

Denmark. 

This work was supported by the Danish Health Insurance 

Foundation, the Danish Heart Foundation, and the Danish Medical 

Research Council. 

Running head: Blood lead and blood pressure 
P.4 

Grandjean et al page 3 

Grandjean, P. (Department of Environmental Medicine, Odense University, 

5000 Odense, Denmark), H.Hollnagel, L.Hedegaard, J.M.Christensen, S. 

Larsen. Blood lead-blood pressure relationships: Alcohol intake and 

hemoglobin as confounders. Am J Epidemiol 1988;...: 

A cohort of 504 men and 548 women born in 1936 and residing in the 

Glostrup area, Denmark, were first seen at age 40, and 451 men and 410 

women underwent a complete re-examination 5 years later. The examinations 

included blood lead concentration and blood pressure assessment under 

careful quality control. The blood lead levels averaged 13 and 9 ug/100 

ml at age 40 and 9 and 6 ug/100 ml at age 45 years in men and women, 

respectively. A slightly increased blood lead was seen in 40-year-old 

women with a systolic blood pressure above 140 mmHg and/or a diastolic 

pressure above 90 mmHg. Systolic blood pressure in men and women and 

diastolic blood pressure in women correlated significantly with log 

blood lead at age 40 years, but not at age 45, a doubling in blood lead 

being associated with an increase in blood pressure of 3 mmHg or less. 

Of nine potential confounders assessed, only blood hemoglobin and alleged 

ilcohol intake were significantly associated with both blood lead and 

lood pressure. If one or both confounders were entered into a multiple 

egression analysis, all associations between blood lead and blood 

ressure became non-significant, in some cases with a negative regression 

coefficient. Also, the blood lead/hemoglobin ratio was poorly associated 

with blood pressure, in particular in individuals with a low alcohol 

intake. As both hemoglobin level and alcohol intake appear to be biologically plausible confounders, any independent effect of low-level lead 

exposure on blood pressure could not be determined. 

alcohol drinking; blood pressure; hemoglobins; hypertension; lead; 

prospective studies. 
P.5 

Grandjean et al. page 4 

Both historical evidence and recent epidemiological studies 

suggest an increased risk of hypertension with excessive blood 

lead levels (1). Of particular public-health interest is the 

finding that this tendency may occur at blood lead levels prevalent in industrialized populations without occupational exposure to lead (2-5). If confirmed, environmental lead pollution 

would be implied as a cause of hypertension in a large number 

of patients. However, a correlation between blood lead levels 

and blood pressures may not necessarily indicate a causal relationship. Although the studies in concert tend to support the 

hypothesis, weaknesses can be identified in each of them, as is 

normal in epidemiological research. Thus, the studies are crosssectional and include different age groups; age adjustments 

have been used, although not necessarily improving the validity 

of the relationship between blood lead and blood pressure. Other 

possible confounders, such as alcohol intake and blood hemoglobin, were not examined and could have influenced the relationship. Alcohol intake may be a significant predictor for blood 

pressure (6,7), and the same holds true for the hemoglobin level 

(8). As blood lead is associated with both alcohol intake (9) 

and hemoglobin (10), these parameters could be important confounders . 

We have examined the relationship between blood lead and 

blood pressure in connection with the population studies in 

Glostrup, Denmark. Data relating to blood pressure and lead 

exposure have previously been published from these studies (9-

13). The 1936 birth cohort from Glostrup has been examined twice, 

at ages 40 and 45 years. Correlations between blood lead and 
Grandjean et al. page 

systolic and diastolic blood pressures can therefore be determined at two points of time. Also, blood pressures at age 45 

years can be related to the blood lead five years previously. 

P.6 

MATERIALS AND METHODS 

A total of 1,052 individuals (504 men and 548 women; 88% 

of the eligible population) were first seen at 40 years of age 

in 1976. All individuals went through a comprehensive physical 

examination, interview and blood chemistry (blood samples taken 

in the morning after a 12-hour fast)(14). Five years later, 966 

individuals were re-examined. Currently, a study of the same 

individuals at age 51 is being carried out. 

Blood for lead analysis was taken in 10-ml polypropylene 

tubes with EDTA (ethylenediaminetetraacetate) as anticoagulant. 

The sampling technique was found to give rise to negligible 

contamination (10). Blood lead was measured in the majority of 

the cohort at both 40 and 45 years of age, i.e., a total of 869 

individuals (454 men and 415 women). The analytical technique 

and the blood lead results at 40 years have been described by 

Olsen et al. (10). The same analytical technique was used for 

the study at 45 years, but the instrumentation was updated 

(Perkin-Elmer AAS model 5000, HGA-500 with deuterium background 

correction). Quality control procedures were included in the 

daily routine (10). For the samples at 45 years, analytical 

quality was secured by analysis of an external reference material 

and by participation in an international interlaboratory comparison study (15). The correlation with other laboratories was 

excellent (r = 0.96). 
P.7 

Grandjean et al. page 6 

Blood pressure measurements at the two examinations were 

performed by the same standardized method according to WHO recommendations (16). We used the mercury sphygmomanometer designed 

at the London School of Hygiene and Tropical Medicine (17); on 

this instrument, the systolic and diastolic pressures are read 

after completion of the test, thus minimizing observer variation 

and bias. Diastolic pressure was determined at the disappearance 

of Korotkoff phase 5. Daily calibration of the instruments was 

carried out, and all blood pressure measurements during the day 

were measured with a 12 x 33 cm cuff and by the same observer 

as described by Hollnagel (18). 

Each participant filled in an extensive questionnaire before 

the examination, and the answers were then reviewed with the 

physician; appropriate groups were used for classification of 

the answers (18). The following parameters from the questionnaire were selected as relevant predictors in relation to lead 

exposure and blood pressure: exercise (three groups), smoking 

(non-smokers, ex-smokers and three groups of smokers), alcohol 

intake (total number of units consumed during the week prior to 

the examination, one unit corresponding to one beer) and occupation (presence or absence of potential lead exposure). Body 

weight was transformed into a height-adjusted weight index given 

in percent of the optimal weight (18). Blood chemistry was 

performed at the Department of Clinical Chemistry at the University Hospital in Glostrup and included blood hemoglobin, serum 

cholesterol and serum triglycerides (18); these parameters were 

selected for confounder analysis as well. 

Blood pressure and a logarithmic transformation of the 
P.8 

Grandjean et al. page 7 

blood lead levels approached a Gaussian distribution. Thus, 

statistical analysis included Pearson's correlation coefficient 

and multiple regression analysis. However, for associations 

with some predictors (exercise, season, smoking and occupational 

exposure), non-parametric tests were used (Kruskal-Wallis oneway analysis of variance and Mann-Whitney U-test). 

RESULTS 

Of the 869 individuals with blood lead results at both 40 

and 45 years of age, complete blood pressure data were available 

for 861 (451 men and 410 women, corresponding to 79% and 66% of 

the eligible population, respectively). The results reported 

below relate to these individuals only, unless otherwise indicated. The median blood lead at age 40 was 13 ug/100 ml in males 

and 9 in females; at age 45 years, the levels had decreased to 

9 in males and 6 ug/100 ml in females. This decrease occurred 

simultaneously with a reduction in the amount of lead additives 

allowed in gasoline. During the five-year interval, average 

blood pressures changed only little, but body weight index 

increased slightly, serum lipids increased, exercise increased, 

smoking decreased, and alcohol intake increased. 

In accordance with international agreements, hypertension 

was defined as a systolic blood pressure at or above 160 mmHg 

and/or a diastolic pressure at or above 95; in healthy individuals, the systolic blood pressure should be at or below 140 

mmHg and the diastolic at or below 90. As the number of patients 

with hypertension was rather small, a combined group was formed 

of all individuals with a blood pressure not considered normal 
P.9 

Grandjean et al. page 8 

according to the above definition. The blood lead levels in men 

and women at ages 40 and 45 years in relation to hypertensive 

treatment and blood pressure classification are shown in tables 

1 and 2. Except for a slightly higher blood lead in women with 

increased blood pressure at age 40 years, the blood lead levels 

appear to vary without any relationship to hypertension. 

Despite the lack of difference in blood lead between hypertensive and non-hypertensive groups, blood lead showed weak, 

but significant associations with systolic and diastolic blood 

pressures, mainly in men. Although statistically significant, 

such correlations could be due to confounding. Thus, when included with the above-mentioned nine predictors in multiple 

regression analyses with blood pressure as dependent variable, 

blood lead showed no significant relationship with blood 

pressure. However, with a multitude of parameters available, 

even relevant correlations may be explained away by spurious 

relationships. 

Confounding bias could be caused if a predictor is meaningfully associated with both blood lead and blood pressure without 

being a link in the causal chain examined. The statistical 

association of relevant predictors with blood lead and blood 

pressures was therefore examined for the 40-year-old men and 

women (table 3). Exercise, season and weight index did not 

correlate with both blood lead and blood pressure and could 

therefore be excluded from further consideration. With increasing 

serum cholesterol or triglycerides, higher blood pressures were 

seen. Surprisingly, blood lead levels also tended to increase. 

Due to the lack of any explanation for this finding, the associa-
P.10 

Grandjean et al page 9 

tion was considered spurious for the purposes of the present 

study. With regard to smoking, the highest blood lead levels 

were seen in the heavy smokers (> 24 g/day, with one cigarette 

corresponding to 1 g of tobacco), while the highest mean blood 

pressures were seen in ex-smokers whose blood lead levels were 

close to average. As blood lead tended to increase with increased 

smoking, and blood pressure did not, smoking was regarded irrelevant with regard to confounding bias. The same applies to 

the slightly lower diastolic blood pressures seen in the small 

number of males in occupations with potential lead exposure. As 

hemoglobin concentration and alcohol intake correlated with 

both blood lead and blood pressure, and these associations 

appeared meaningful, these potential confounders were selected 

for a detailed analysis. 

The increase in blood pressure associated with a doubling 

in blood lead is shown in tables 4-6. This increase is calculated by multiplying the regression coefficient for log blood 

lead vs blood pressure by 0.3010. The regression coefficients 

were determined separately for the data at 40 years, at 45 years, 

and for the data at 45 years with blood lead at age 40. Both 

confounders generally correlated better with blood pressure 

than did blood lead. When one or both of the two potential 

confounders were included in the regression analysis, any statistical significance of the relationship between blood lead and 

blood pressure was lost. 

Alcohol intake tended to become an insignificant predictor 

for blood pressure when blood lead was forced as the first 

independent variable. Blood hemoglobin remained significant in 
P.11 

Grandjean et al. page 10 

all analyses, except for diastolic pressure in 45-year-old women 

where hemoglobin became an insignificant predictor if entered 

after blood lead. With diastolic blood pressure in 40-year-old 

males (table 4), adjustment for hemoglobin resulted in a negative, though not statistically significant, regression coefficient for blood lead. This observation may suggest that, when 

entering hemoglobin into the regression analysis before blood 

lead, an overadjustment may result. 

An additional series of analyses was therefore carried out 

using the ratio between blood lead and hemoglobin as the independent variable. Again, this parameter showed a poorer correlation 

with blood pressure than did the unadjusted blood lead, though 

somewhat better than blood lead after introduction of hemoglobin 

in the regression analysis. Thus, the correlation with systolic 

and diastolic blood pressure in 40-year-old women approached 

statistical significance (p < 0.1) with predicted increases of 

2.4 and 1.9 mmHg, respectively, for each doubling of the lead/-

hemoglobin ratio (cf. table 4). 

This analysis was then repeated for the individuals who 

had ingested less than 7 units of alcohol during the week prior 

to the examination. In the 176 male abstainers or light drinkers 

at age 40 years, a doubling of the lead/hemoglobin ratio was 

associated with a significant decrease in diastolic blood 

pressure of 4.7 mmHg (p < 0.05); the same tendency, though nonsignificant, was already observed in the total group of 451 men 

(table 4). In contrast to this reverse relationship, the comparable group of 317 women at the same age showed an increase 

in diastolic blood pressure of 2.3 mmHg with a doubled lead/ 
Grandjean et al. page 11 

hemoglobin ratio (p < 0.1); this increase is higher than the 

one associated with a doubling in unadjusted blood lead (table 

4). All other regression coefficients were non-significant. 

P.12 

DISCUSSION 

The association between blood lead and blood pressure seen 

in the present study is similar to or slightly weaker than those 

reported in previous population studies (2-5). A weaker association could partly be due to the very low blood lead levels in 

Denmark, in particular at the time of re-examination of the 

population. Also, any strong relationship would not be expected 

at ages 40 and 45 years where the prevalence of hypertension is 

fairly low. The homogeneous character of the cohort at welldefined ages would tend tb support the reliability the results, 

as would the fact that nine potential confounders were evaluated. 

The internal validity of the findings is supported by the similarity of the results at two examinations five years apart. On 

the other hand, non-response and loss to follow-up may have influenced the study outcome, although this weakness is not unique. 

Also, the statistical power of a study of less than 1,000 individuals is perhaps not sufficient when dealing with small differences. In addition, the logarithmic transformation of the 

blood lead data imposes a non-linear relationship to blood 

pressures, the biological plausibility of which remains to be 

determined. However, a similar transformation has been used in 

other population studies and comparison is therefore facilitated. 

The major observation in this study is that blood hemoglobin 

and alleged alcohol consumption may cause confounding bias. 
P.13 

Grandjean et al. page 12 

After inclusion of the two parameters in a multiple regression 

analysis, associations between blood lead and blood pressure 

were no longer statistically significant. However, the biological 

validity of such possible confounding should be carefully 

assessed. 

That blood lead tends to increase with the number of units 

of alcohol consumed during the last 7 days has previously been 

documented in the same cohort at 40 years of age; the increase 

is also related to smoking (which in turn is related to alcohol 

consumption) (9). This association was subsequently confirmed, 

eg., in a British study (19) and may be due to alcohol-related 

changes in lead metabolism and/or lead present in some alcoholic 

beverages, in particular wine. Alcohol has significant and 

deleterious physiologic and biochemical effects on the heart 

and has been identified as a risk factor for hypertension (20). 

Alcohol intake was significantly associated with systolic and 

diastolic blood pressures in the NHANES I study (8). Additional 

epidemiological studies have also shown an association between 

alcohol intake and blood pressure (6,7,11,21). However, the 

association may not be linear (22), and the effect of low alcohol 

intake on blood pressure is still unclear. Thus, available 

evidence supports the notion that at least high alcohol intake 

is an independent cause of increased blood pressure and also of 

increased blood lead levels; it is therefore a likely confounder for the blood lead-blood pressure relationship. To illustrate 

this further, an average consumption of 30 ml of ethanol per 

day in one study appeared to produce an increase of 2-6 mmHg in 

systolic blood pressure (6). An alcohol consumption of this 
P.M 

Grandjean et al. page 13 

magnitude would cause an increase in blood lead levels of about 

1.5 ug/100 ml in males and somewhat more in females (9). 

Similarly, the biological plausibility for hemoglobin as 

a confounder must be critically assessed. Although this parameter 

appeared to be the most important confounder, less extensive 

information is at hand to examine the possible mechanisms involved. Almost all lead in the blood is bound to the erythrocytes, and misleadingly low blood lead levels may be seen in 

anemia; adjustment of blood lead to a certain hemoglobin level 

is therefore appropriate. Some laboratories report lead concentrations in relation to erythrocyte, rather than whole blood 

volume. Accordingly, a high hemoglobin was associated with a 

slightly increased blood lead in the Danish cohort when examined 

at 40 years of age (10). This relationship simply indicates 

that a higher proportion of the body burden of lead is carried 

by the erythrocytes, not that the lead exposure was greater. 

Further, increased hemoglobin may be an important risk factor 

for hypertension. Again, the NHANES I study documented a significant correlation between hemoglobin and blood pressure (8), and 

the same tendency was seen in the NHANES II (3). Further, in 

the Framingham study, changes in hematocrit were significantly 

associated with changes in blood pressure in men, though not in 

women (23). Although this correlation could be due to changes 

in blood viscosity, both hemoglobin and blood pressure are also 

related to body size, and the relationship could be an indirect 

one. Thus, as hemoglobin is apparently associated with blood 

lead and blood pressure by independent mechanisms, confounding 

would be expected. 
P.15 

Grandjean et al. page 14 

The biological relevance of the two predictors assessed 

would therefore suggest that the statistically significant 

association between blood lead and blood pressure in the present 

study could be at least partially explained by confounding bias. 

However, a causal role of low-level lead exposure with regard 

to a small increase in blood pressure cannot be ruled out. In 

other studies with less confounding bias, blood lead could well 

be an important predictor for blood pressure. 

The evidence that low-level lead exposures may cause an 

increased blood pressure mainly relates to cross-sectional data 

on individuals at different ages (2-5). Adjustment for age, 

body weight, etc. was included in the analyses, and the regression coefficients found were similar to those seen for the 

unadjusted data in the present study. However, the significance 

of hemoglobin and alcohol as possible confounders cannot be 

determined from the published data, and the validity of the 

associations found in the previous population studies (2-5) is 

therefore unclear. 

Other studies have shown a relationship between occupational 

lead exposure and increased blood pressure (24,25). Despite the 

small numbers and the possible selection bias in studies in 

occupational epidemiology, the evidence is suggestive of a causal 

relationship. Further, in a case-referent study (26), a significantly increased number of hypertensive patients had a blood 

lead level above 2 umol/1 (41 ug/100 ml). In contrast, the 

present study dealt with much lower blood lead levels, but 

potential occupational exposure to lead in a small number of 

individuals was associated with a slightly decreased blood 
Grandjean et al. page 15 

pressure. The same reverse tendency has been reported for a 

larger group of lead-exposed workers (21). 

The experimental evidence is growing that lead may cause 

a range of pathological changes which may be associated with 

an increased blood pressure (1). The hypothesis that this effect 

may also occur in humans is therefore plausible, but the publichealth significance of such a relationship, should it exist, 

cannot be determined at this time. 

In conclusion, the present study has shown that lead exposure is related to increased blood pressure. However, the 

statistical significance of this association disappears when 

alcohol intake and hemoglobin are included in a multiple regression analysis. Both parameters are plausible confounding 

factors and need to be carefully controlled to assess the character of the blood lead-blood pressure relationship. 
P.17 

Grandjean et al page 16 

References 

1. U.S Environmental Protection Agency. Lead effects on cardiovascular function, early development, and stature: An addendum 

to U.S. EPA Air quality criteria for lead (1986)(EPA-600/8-

83/028aF, Vol. 1). Research Triangle Park, NC: 1986. 

2. Kromhout D, Wibowo AAE, Herber RFM et al. Trace metals and 

coronary heart disease risk indicators in 152 elderly men (the 

Zutphen study). Am J Epidemiol 1985; 122: 378-85. 

3. Pirkle JL, Schwartz J, Landis JR et al. The relationship 

between blood lead levels and blood pressure and its cardiovascular risk implications. Am J Epidemiol 1985; 121: 246-58. 

4. Pocock SJ, Shaper AG, Ashby D et al. Blood lead concentration, 

blood pressure and renal function. Br Med J 1984; 289: 872-4. 

5. Pocock SJ, Shaper AG, Ashby D et al. Blood lead and blood 

pressure in middle-aged men. In: Lekkas TD, ed. Heavy metals 

in the environment, Vol. 1. Edinburgh: CEP Consultants, 1985: 

303-5. 

6. Criqui MH, Wallace RB, Mishkel M et al. Alcohol consumption 

and blood pressure. Hypertension 1981; 3: 557-65. 

7. Klatsky AL, Friedman GD, Siegelaub AB et al. Alcohol consumption and blood pressure. N Engl J Med 1977; 296: 1194-1200. 

8. Harlan WR, Hull AL, Schmouder RL et al. Blood pressure and 

nutrition in adults, The National Health and Nutrition Survey. 

Am J Epidemiol 1984; 120: 17-28. 

9. Grandjean P, Olsen NB, Hollnagel H. Influence of smoking and 

alcohol consumption on blood lead levels. Int Arch Occup Environ 

Health 1981; 48: 391-197. 
P.18 

Grandjean et al. page 17 

10. Olsen NB, Hollnagel H, Grandjean P. Indicators of lead 

exposure in an adult Danish suburban population. Dan Med Bull 

1981; 28:168-76. 

11. Ibsen H, Christensen NJ, Rasmussen S et al. The influence 

of chronic high alcohol intake on blood pressure, plasma noradrenaline concentration and plasma renin concentration. Clin 

Sci 1981; 61: 377s-9s. 

12. Schroll M. A ten-year prospective study, 1964-1974, of 

cardiovascular risk factors in men and women from the Glostrup 

population born in 1914. Dan Med Bull 1982; 29: 213-52. 

13. Schroll M, Kirkby H, Kirchhoff M. Arterial hypertension as 

a risk factor for cerebrovascular disease. 15-years follow-up 

of the 1914-population in Glostrup. Acta Med Scand 1983; 676: 

33-36. 

14. Hollnagel H. The health structure of 40-year old men and 

women in the Glostrup area, Denmark. An epidemiological survey. 

Dan Med Bull 1980; 27: 121-30. 

15. Berlin A. Assessment of exposure to lead of the general 

population in the European community through physiological 

monitoring. Environ Monitor Assess 1982; 2: 225-31. 

16. Rose GA, Blackburn H. Cardiovascular survey methods. (WHO 

monograph series 56). Geneva: World Health Organization, 1968. 

17. Rose GA, Holland WW, Crowley EA. A sphygmomanometer for 

epidemiologists. Lancet 1964; 1: 296. 

18. Hollnagel H. The health structure of 40-year-old men and 

women in the Glostrup area, Denmark - an epidemiological survey. 

Dan Med Bull 1980; 27: 121-30. 

19. Pocock SJ, Shaper AG, Walker M et al. Effects of tap water 
P.19 

Grandjean et al page 18 

lead, water hardness, alcohol, and cigarettes on blood lead 

concentrations. J Epidemiol Comm Health 1983; 37: 1-7. 

20. Segel LD, Klausner SC, Gnadt JTH et al. Alcohol and the 

heart. Med Clin North America 1984; 68: 147-61. 

21. Parkinson DK, Hodgson MJ, Bromet EJ et al. Occupational 

lead exposure and blood pressure. Br J Ind Med 1987;44:744-8. 

22. Jackson R, Stewart A, Beaglehole R et al. Alcohol consumption and blood pressure. Am J Epidemiol 1985; 122: 1037-44. 

23. Kannel WB, Sorlie P. Hypertension in Framingham. In: Paul 

O, ed. Epidemiology and control of hypertension. New York: 

Stratton, 1975: 553-92. 

24. Kort, WLAM de, Verschoor MA, Wibowo AAE et al. Occupational 

exposure to lead and blood pressure: A study in 105 workers. 

Am J Ind Med 1987; 11: 145-56. 

25. Kirkby H, Nielsen CJ, Nielsen VK et al. Health examination 

of persons with long-term occupational exposure to lead (in 

Danish). Ugeskr Lag 1987; 149: 942-5. 

26. Beevers DG, Erskine E, Robertson M et al. Blood lead and 

hypertension. Lancet 1976; 2: 1-3. 
P.20 

Grandjean et al. page 19 

Table 1 

Median blood lead level (in ug/100 ml) (10th and 90th 

percentiles in parenthesis) in 454 men and 415 women 

at age 40 years in relation to hypertensive treatment 

and blood-pressure classification 

Men Women 

Number Blood lead Number Blood lead 

Treatment 

No treatment 

Increased blood pressure 59 

Normal blood pressure 

5 

449 

59 

392 

11 

13 

13 

13 

(9-17) 

(8-20) 

(8-21) 

(8-20) 

11 

402 

19 

391 

9 (5-13) 

9 (6-13) 

10*(5-23) 

9 (6-13) 

p < 0.05 (Mann-Whitney U-test) 

iv.. 
P.21 

Grandjean et al page 20 

Table 2 

Median blood lead level (in ug/100 ml) (10th and 90th 

percentiles in parenthesis) in 454 men and 415 women 

at age 45 years in relation to hypertensive treatment 

and blood-pressure classification 

Men Women 

Number Blood lead Number Blood lead 

Treatment 

No treatment 

Increased blood pressure 44 

Normal blood pressure 

18 

435 

44 

410 

10 

9 

9 

9 

(5-13) 

(5-14) 

(5-15) 

(4-14) 

21 

392 

17 

396 

6 

6 

6 

6 

(4-9) 

(4-10) 

(5-14) 

(4-10) 
Grandjean et al. page 21 

Table 3 

Statistical significance for association of potential 

confounders with blood pressure (BP) and blood lead 

in 451 men and 410 women aged 40 years 

Confounder 

Exercise* 

Season+ 

Weight index§ 

Cholesterol^ 

Triglycerides§ 

Smoking4" 

Occupational exp." 

Hemoglobin^ 

Alcohol§ 

Systol 

Men 

NS 

NS 

*** 

• 

** 

NS 

NS 

** 

• 

.ic BP 

Women 

NS 

NS 

*** 

NS 

*** 

NS 

NS 

*** 

** 

Dias 

Men 

NS 

NS 

• * * 

*** 

*** 

** 

* 

*** 

** 

tolic BP 

Women 

NS 

NS 

• * * 

NS 

NS 

NS 

NS 

NS 

NS 

Blood 

Men 

NS 

• • • 

NS 

* • * 

** 

* • * 

* • 

* ** 

• * * 

lead 

Women 

NS 

*** 

NS 

NS 

** 

* 

* 

* • * 

*** 

i 

j 

i 

Statistical significance determined by

 +Kruskal-Wallis oneway analysis of variance, §Pearson's correlation coefficient, and 

"Mann-Whitney U-test 

*p < 0.05; **p < 0.01; ***p < 0.001; NS p > 0.1 
Grandjean et al. page 22 

Table 4 

Increase in blood pressure (BP in mmHg) with a doubling 

in blood lead in 451 men and 410 women at age 40 years, 

as adjusted for possible confounders'*' 

Systolic BP Diastolic BP 

Men Women Men Women 

Unadjusted 

Adjusted for: 

alcohol intake 

hemoglobin 

both 

2.6' 

2.0 

1.5 

1.1 

3.T 

1.8 

1.9 -1.0 

-1.6 

2.1' 

1.6 

1.7 

1.2 

+only indicated if p < 0.5; *p < 0.05 
Grandjean et al. page 23 

Table 5 

Increase in blood pressure (BP in mmHg) with a doubling 

in blood lead in 451 men and 410 women when re-examined 

at age 45 years, as adjusted for possible confounders'*' 

Systolic BP Diastolic BP 

Men Women Men Women 

Unadjusted 

Adjusted for: 

alcohol intake 

hemoglobin 

both 

2.2 

1 .2 

1.3 

_ 

1.1 

0.6 

1.3 

1 .2 

1 .2 

1.0 

+only indicated if p < 0.5 
P.25 

L 

Grandjean et al. page 24 

Table 6 

Increase in blood pressure (BP in mmHg) in 451 men and 410 women 

at age 45, as related to a doubling in blood lead at age 40 

and adjusted for possible confounders at age 45 years"*" 

Systolic BP Diastolic BP 

Men Women Men Women 

Unadjusted 

Adjusted for: 

alcohol intake 

hemoglobin 

both 

3.0" 

2.3 

2.1 

1.4 

2.3 

2.2 

2.2 

_ 

1.1 

0.7 

0.7 

+only indicated if p < 0.5; *p < 0.05