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Effects of sub-clinical levels of lead in children.




Levels of blood lead in Australian children

Sources of lead in children

Inhalation of atmospheric lead

Lead in dusts

Food and drink

Effects of sub-clinical levels of lead in children

Reducing lead uptake in children

Some concluding points




Although obvious symptoms of severe lead poisoning in children such as vomiting and paralysis were first described in Australia 100 years ago, it was only in the late 1980s that US researchers provided strong evidence for harmful and lasting effects of mild lead poisoning in children. In particular, it was discovered that mental development at the toddler stage was hindered to a small but measurable degree when quite low levels of lead were present in children's blood.

In 1991 the US accepted the validity of the above research and lowered its upper limit of blood lead in children. This action sparked increasing concern in Australia, resulting in the lowering of this country's own lead 'level of concern' down to the US level in June 1993. Secondly, a Federal Government-sponsored roundtable conference held in July 1993 set targets for oil refineries to reduce the amount of lead used in petrol. Thirdly, the 1993-94 Federal Budget provided for an increase in the price of leaded (high-octane, 'super') petrol compared with unleaded petrol. Lastly, the Federal Government is about to embark on a lead abatement campaign directed from CEPA, the Commonwealth Environment Protection Agency.

This short paper describes what is known about blood lead levels in young Australian children and summarises the evidence for sub-clinical (hidden) effects of lead in the first years of life. Not surprisingly, the highest blood lead levels have been found in cities such as Pt Pirie and Broken Hill which have had large lead-based industries operating over a long period. Much less information is available on lead in children living in ordinary suburbs and inner city areas away from lead industries. Such children could be expected to be receiving much of their lead intake from lead in petrol. Screening data post 1985-86, when unleaded petrol was first made mandatory for new cars, is particularly meagre. However, it has been assumed from this and overseas data that about 45 per cent of young children in Australia have blood levels exceeding the new level of concern, namely, 10 micrograms lead per decilitre blood.

Concerning the sub-clinical effects of lead, it is now believed by scientists that intelligence, hearing, stature, steadiness and birth weight can all be significantly impaired by low blood levels in the young child. There seems to be no lower threshold for these to occur, although measurement of both lead and IQ, etc., becomes difficult below 10 micrograms lead per decilitre of blood. At levels above 30 micrograms per decilitre, the impairment of intelligence may be sufficient to prevent a child reaching university standard.

The harm lead causes to mental development can be a relatively small factor compared with other environmental and genetic influences. However, the largely irreversible effects of lead should be preventable with suitable lead abatement policies.

The paper is concluded with a reminder that, overall, very little is known of Australian children's exposure to lead; however, this is insufficient reason for inaction on the lead-in-petrol question. As well as the change to somewhat more expensive leaded as compared with unleaded petrol in order to lower demand, oil refineries should be persuaded to examine a number of available options for reducing lead while maintaining the octane level of petrol for use in older cars.


Australia gets an honourable mention in textbooks on lead pollution for the reason that lead poisoning in children was first described 100 years ago in Queensland. 1 The clinical symptoms include persistent vomiting, headaches, eye problems, convulsions and partial paralysis. Certain underlying biochemical effects of lead can also be measured. Although ingestion of lead-based house paint was correctly blamed for the Queensland poisonings, and although certain leaded paints were later banned there, the detective work was ahead of its time. For example, it was not until the 1950s and 1960s that possible causes for childhood lead poisoning were examined in American cities.

In human health terms, lead compounds have always been insidious substances. Lead has no biochemical role in the body and is harmful essentially because it interferes with enzymic activity. Not surprisingly, the generally accepted ideal level in human beings is zero 2 .

Young children are more subject to lead poisoning than adults because they absorb about 50 per cent of all lead swallowed. The corresponding figure for adults is only 8-10 per cent 3 . Other reasons for children's greater susceptibility include foetal uptake of lead from the mother before birth, their developing nervous system which is especially sensitive to lead, their smaller body size (greater lead concentrations, all else being equal) and their greater exposure to environmental lead through play and habits such as finger-sucking.

From the late 1960s, the level of blood lead in children considered to be safe has been steadily decreasing. In the US, the declared upper limit was reduced from 60 micrograms per decilitre (micro g/dl) to 40 micro g/dl in 1970, to 30 micro g/dl in 1975, to 25 micro g/dl in 1985 and to 10 micro g/dl in 1991. Australia's National Health and Medical Research Council (NHMRC) set its own 'level of concern' at 30micro g/dl in 1979; then reduced it to 25 micro g/dl in 1987; and now (1993) has a new upper limit of 10 micro g/dl. While a level of 40-60 micro g lead /dl or above in children gives rise to clear clinical symptoms, very few children now become hospitalised with obvious lead poisoning (e.g., about one per year at the Children's Hospital in Sydney 4 ), so attention is mainly directed towards sub-clinical effects of lead.

While concern over lead uptake in children has intensified in Australia over the past eighteen months or so, the 1993-94 Budget provision for higher taxes on leaded compared with unleaded petrol brought the issue of lead poisoning of children into national prominence. The following paper provides a summary of the more important published data on sub-clinical lead in children, including levels, sources and effects. This information is an essential input for the lead-in-petrol debate.

Levels of blood lead in Australian children

The world's best-known example of environmental pollution by lead is Pt Pirie in South Australia, where a lead smelter has operated for over 100 years. In 1985 5 the large Port Pirie Cohort Study reported blood lead levels in over 600 children born there between 1979 and 1982 (more on the Study later). Average lead levels increased in subjects up to 2 years of age to a maximum value of about 21 micro g/dl, then gradually declined with age. An earlier study by the South Australian Health Commission 6 had found a similar maximum value; beyond 4 years of age the lead blood levels had continued to decline to an average of about 16 micro g/dl at age 10. Virtually no difference in lead uptake was apparent between girls and boys in either study.

Other major lead industry activities have been carried out at Pt Kembla and Broken Hill. In the case of the former city, a 1990 survey of 83 children aged 3 years and living downwind of the lead smelter there showed lead blood levels greater than 15micro g/dl in two-thirds of them 7 . In October 1991 the NSW Health Department revealed that over one-third of 230 pre-schoolers living in South Broken Hill exceeded 25 micro g/dl blood lead (the contemporary Australian standard), and more than two-thirds exceeded a level of 10 micro g/dl. 8

The most recent concerns in Australia over lead intake by children arise from measurements of blood lead in inner city areas. A 1991 NSW Health Department survey of 49 young Balmain children showed the following 9 :

51 per cent equalled or exceeded 10 micro g/dl

12 per cent 15 micro g/dl and

2 per cent 25 micro g/dl blood lead.

Note that the children were chosen from 1000 houses 'in an area known to have a large amount of lead in the environment from previous industrial uses, high traffic volume and many houses decorated with paint containing lead'. 10 Similar results were obtained in the Summer Hill area of Sydney where 46 children were tested:

41 per cent equalled or exceeded 10 micro g/dl

13 per cent 15 micro g/dl and

2 per cent 25 micro g/dl blood lead.

By contrast, The Melbourne Age of 29.7.93 and The Canberra Times of 5.8.93 reported on a very recent study of 130 Victorian children which found that average blood lead levels had fallen by half (from 10.5 to 5.2 micro g/dl) since 1979 when previous testing had been done, and also found that there was no statistical difference between blood lead levels for urban and rural children. Early indications were that up to 96 per cent of Victorian children may have lead levels below 10 micro g/dl, the new Australian level of concern.

Nation-wide screening for blood lead such as was carried out in the US from 1976 to 1980 has not been attempted in Australia, and very little has been spent here on the testing of children outside major lead industry areas in the last five years or so. The screening carried out has been relatively isolated, and varying in size, methodology and sophistication. However, these existing Australian studies together with overseas data have been taken as suggesting that a large proportion of children in this country aged 0-4 years - thought by some experts to number between 310,000 and 630,000 11 - have blood lead in excess of the new concern level of 10 micro g/dl; on present evidence, much smaller numbers approach or exceed the former Australian limit of 25 micro g/dl. Current estimates of percentages of Australian children having various blood lead levels are given below. 12

Table no available online

Because so many children are thought to fall between two levels, i.e., 10 and 25 micro g/dl, it has been considered necessary to ascertain the harmful effects of lead at levels within that range, and devise policies for the further reduction of lead in the human environment.

Sources of lead in children

Unlike many other pollutants, lead enters the human body in various ways and from many sources. It should also be remembered that lead is an element and does not chemically break down to harmless substances as do many pesticides, for example.

While several applications of lead compounds (such as pigments in house paints) have been phased out, lead remains a very useful element and Australia is the leading world producer. The major sources of environmental lead pollution are lead mining and smelting; and leaded petrol. But there is a host of other sources including emissions from lead recovery plants, battery factories, foundries, soldering works, cable sheathing and incineration. People can be exposed to lead from old paints, food, beverages, some china glazes, and from lead crystal glass. This section summarises the most common pathways to human uptake.

Inhalation of atmospheric lead

It is generally accepted (for example, Ref. 13 ) that about 90 per cent of atmospheric lead is from leaded petrol. Figure 1 below illustrates this by showing a close US correlation between the amount of lead used in petrol and levels of lead measured in the air.

While some lead from petrol is released in a vapour-phase organic form (during manufacture and from evaporation), exhaust lead gives rise to inorganic particulate lead in the form of a very fine aerosol of various lead halides (chlorides, bromides, etc.), which subsequently form lead acids, carbonates or sulphides. The organic lead follows a similar chemical route.

Breathing city air is an involuntary action and therefore continuously exposes the lungs to lead. It is estimated that 40-50 per cent of inhaled atmospheric lead becomes absorbed in the breathing apparatus. Nevertheless, breathing in atmospheric lead is considered a relatively minor pathway of lead uptake, perhaps 7-8 per cent of the total absorbed by a young child 14 . Blood lead levels have a relationship with, but do not correlate strongly with levels of lead in air.

Figure 1 not available online

Lead in dusts

Lead from many sources tends to accumulate in dusts; knowledge of this fact is crucial to reduction of children's exposure in inner city housing. Apart from their special risk in, say, Pt Pirie and Broken Hill, lead-containing dusts are most likely to arise from old paints powdering, flaking or being removed by sanding, burning or blasting; and from the wet and dry deposition of atmospheric lead from vehicle exhausts. Dust ingestion probably accounts for at least 35 per cent of a city child's lead intake 15 , but the figure in individual cases could be much higher. The Port Pirie Cohort Study found a strong correlation between blood lead concentrations and lead levels in surface soils 16 .

Not surprisingly, soils near main roads and old houses show higher levels of lead than elsewhere in cities. Whereas uncontaminated soil might be expected to contain 10-50 parts per million (ppm) lead, soils alongside busy roads typically record 50-2000 ppm lead. In 1988, levels of up to 7030 ppm lead were found in Balmain soils 17 and thus identified the locality as a potentially high-risk area. Lead never breaks down in soils and dusts, so the danger of poisoning can persist long after the source is removed.

It would be of great interest to know with some certainty the proportion of environmental lead deriving from leaded petrol alone; the figure is probably a significant one. Whereas the higher values of urban child blood lead levels (25 micro g/dl or more) may well be augmented by some special point source such as old leaded paints or a lead-related industry, the more common levels found such as 5-15 micro g/dl are likely to be depending (to an unknown extent) on the continued use of leaded petrol.

An elegant experiment has been described 18 in which the isotope ratio of lead Pb 206: Pb 207 in leaded petrol was slowly changed with the cooperation of Italian oil companies over a period of 6 years. During this period both the atmospheric and the blood lead isotope ratio in residents of Turin was monitored. Significantly, variation of the ratio in petrol was followed by a corresponding change in isotope ratio in the atmosphere and in people.

Although Australian data is inadequate to determine whether blood lead levels here are related to levels of lead in petrol, the US Centers for Disease Control (CDC) data shown below (fig. 2) was collected at the period of greatest fall in the overall lead content of petrol sold in that country. The correspondence between lead used and lead in blood is remarkable, and has been accepted as strong evidence for blaming leaded petrol for much lead uptake in children.

Figure 2 not available online

Food and drink

This category has usually been considered to account for as much as 50 per cent of a child's lead intake. However, one of the most important sources of lead in food, namely lead-soldered cans, has been almost eliminated by Australian manufacturers using a more modern welding technology. Uptake of lead in children from food should therefore be on the decline. Recently, the National Food Authority arranged for a study of lead in canned food, with an emphasis on imported soldered cans. It was found that the soldering process increased the levels of lead in food by a factor of nine, prompting a call for tighter Australian standards which would be easily met by welded cans.

Lead in food tends to be an additive process, being commenced during the growing of vegetables (polluted air, water and soils), and continuing over the various processing steps including canning. In the home, lead can enter food via house dusts or, more rarely, through the action of acidic foods or drinks on lead-based glazes on ceramic containers.

As mentioned earlier, children absorb a much higher proportion of swallowed lead than do adults, but note that lead is not as bioaccumulative throughout the food chain as is mercury, for example. Lead absorption is known to be accelerated in experimental animals by dietary deficiencies of calcium, iron, zinc, copper and Vitamin D 19 . One can imagine a high-risk inner-city scenario where a young child might be deficient in, say, calcium and iron, and be heavily exposed to lead absorption from food, old house paint (worn or being sanded off) as well as atmospheric lead and contaminated soils deriving from leaded petrol.

Finally, lead may be absorbed into the body by drinking lead-polluted water or, more importantly, processed drinks such as carbonated beverages containing lead.

Effects of sub-clinical levels of lead in children

It was long believed by doctors (up to about 1970) that no harmful effects persisted in children after treatment for lead poisoning and when clinical signs had disappeared. It was further believed that a child having blood lead levels below about 40 micro g/dl was not liable to be affected in any way.

These claims were first challenged 50 years ago by Byers and Lord, who followed up 20 'cured' lead-poisoned children and found that 19 had reading, learning and behaviour defects, and were having problems with their schooling. It was argued by Byers and Lord that lead neurotoxicity might not be limited to brain haemorrhage and cell death, but could be inhibiting normal growth of the nervous system in children.

Larger, more comprehensive follow-up studies were undertaken in the 1970s, culminating in the survey and follow-up of 270 Boston children by Herbert Needleman 20 . None of the children showed any signs of classical lead poisoning; their cumulative lead exposure was estimated by measuring lead levels in teeth. Needleman produced evidence - which did not go unchallenged - that the mental performance of young children falls off as higher dentine lead levels are recorded. Furthermore, such losses in performance appeared to persist in the same children 11 years later 21 . Figures 3 and 4 below give results from a number of reports linking lead levels to intelligence in children.

Figures 3 and 4 not available online

Foetal exposure as well as childhood exposure to lead at 'low' levels (10-25 micro g/dl in blood) seems to affect mental development. Studies of 300 families in a low socio-economic area of Cincinnati and 249 infants from middle and upper income families in Boston 22 have revealed that children with the highest umbilical-cord blood lead at birth score worst in standardised verbal, reading, puzzle completion and hand-eye coordination tests. Australian scientists are currently planning to measure the transfer of bone lead from mother to foetus. Bone is a major repository of lead in the body.

The previously mentioned Port Pirie Cohort Study is the largest of all. 23 Starting with a large group of pregnant women living in or near Pt Pirie, researchers from the University of Adelaide, CSIRO, the University of Newcastle and other institutions measured the women's blood lead during pregnancy and at delivery; their children's blood lead at 6, 15 and 24 months of age; and each year afterwards up to the age of 7. Standard psychological tests were administered to the children at age 2, 4 and 7 years.

All age groups examined have a poorer average mental performance in the higher blood lead brackets. For example, the four-year-olds with an average 32 micro g/dl scored 7 per cent lower than those with an average of 10 micro g/dl. That mental development was not merely being delayed by lead is shown in the follow-up of seven-year-olds, whose measured IQ was still about 5 per cent less in those children who had 30 micro g/dl blood lead at age 3 compared with those having 10 micro g/dl. Lead at these 'low levels' also affects hearing, stature, steadiness and birth weight. 24 An important conclusion arising from Australian, Boston and Cincinnati results is that there seems to be no obvious threshold below which exposure to lead is totally without effect.

The main objection to the above type of study, both in Australia and elsewhere, is that the influence of family or environmental factors apart from lead might be sufficient to account for the findings. For example, lead exposure may be occurring coincidentally in families who have below average children for a variety of other reasons such as occupation and IQ of parents, etc. While the researchers agree that lead may well be a minor influence on mental development compared to other childhood influences, they maintain that application of correction factors for parents' occupations, etc., has failed to eliminate an effect of lead itself. Meanwhile, the thrust of Needleman's work has largely been accepted by US health authorities, leading to adoption of the new US limit of 10 micro g/dl blood lead in October 1991.

It could be argued from the epidemiological work that the difference in expected mental ability of two children having, say, 9 and 15 micro g/dl blood lead at the toddler stage only amounts to one or two IQ points at most. It should be remembered, however, that the study results have been expressed as averages; therefore, the spread of scores encompasses individuals who have been affected more than average. Secondly, blood levels of 30 micro g/dl and more are thought to cause major disadvantages such as reducing the ability of a child to reach university standard. Thirdly, there is some evidence that less advantaged families are more at risk from lead poisoning, which once again may be hidden in an average score with family factors such as poverty 'corrected for'. Lastly, while the mental handicap observed at the very lowest lead levels may appear small in an individual, it may well be significant and costly when the whole population is considered.

An International Meeting in Melbourne on Non-Occupational Exposures to Lead held in October 1992 concluded that young children are likely to lose between 0 and 5 IQ points for each 10 micro g/dl lead increase in blood between 10 and 25 micro g/dl, with an average of 2-3 IQ points. Above a level of 25 micro g/dl the rate of intelligence loss may be greater, while errors in measurement of intelligence and lead exposure within the range 0-10 micro g/dl are too large to determine any effects on children 25 .

Reducing lead uptake in children

If it is accepted that urban children in Australia have blood lead levels which are generally too high - though screening data is so far quite inadequate - then policies for the reduction of lead uptake need to be considered. The decision in June 1993 by the NHMRC to lower its lead in blood level of concern from 25 micro g/dl to 10 micro g/dl should be having the effect of alerting parents and governments to the effects of sub-clinical lead levels in children, and should be setting in train both education and lead reduction programs where they are necessary. The Commonwealth Environment Protection Agency is presently developing a national lead abatement strategy.

Common-sense guidelines are available for lead poisoning prevention in the inner-city and/or roadside home. For example:

exposed dirt in backyards should be minimised;

fruit and vegetables should be thoroughly washed before use;

children's hands should be frequently washed, especially before mealtimes;

homes should be regularly cleaned with water or steam as well as simple vacuuming (which merely returns finer particles to the air), with particular attention to areas where dust can accumulate;

lead absorption into the body is reduced by a low-fat diet adequate in calcium, iron and zinc;

pets should be regularly washed;

children should be discouraged from playing in dirt or dust; and

there should be total exclusion of pregnant women and young children from old houses being renovated, especially if lead-based paint is known to be present.

Since leaded petrol appears to be responsible for much or most of the remaining environmental lead in cities without a major lead industry, it would seem advisable to develop policies to eliminate this source in particular. Although unleaded petrol was introduced to Australia in 1985-86, and although all new cars have since been required to use this fuel, the phaseout of leaded petrol is proceeding much slower than originally intended. In fact, leaded fuel is expected to continue to outsell unleaded fuel up to 1994, according to the latest estimates. At this rate a total phaseout could not be expected until 2005 or even later.

The well-known reason for leaded petrol remaining dominant up to now is that Australia's existing vehicle fleet is ageing while the new car market is sluggish. Australian Bureau of Statistics 1991 figures show that passenger cars on the road and manufactured before 1986 make up nearly three-quarters of the total fleet. Furthermore, the ageing trend is worsening year by year. Many of these older cars cannot use low-octane unleaded fuel without adversely affecting pollution, power, wear and economy.

Detailed discussion of the lead-in-petrol question is beyond the scope of this paper. However, the high levels of lead allowed in Australian leaded petrols should be noted. For example, 0.3 grams/litre maximum in Victoria is the lowest in Australia but still compares unfavourably with a maximum of 0.15 g/l in many European countries, and much less again in Canada and the US. One could argue on this basis alone that the Australian States and Territories should standardise maximum lead levels in petrol to at least 0.15 g/l in line with common overseas practice. An NHMRC-funded study team, 26 the NRMA and the Australian Conservation Foundation have in fact recommended such action, but the July 1993 Roundtable Conference on Lead agreed to more relaxed targets for oil companies: 0.2 g/l in Sydney and Melbourne and 0.3 g/l elsewhere by the end of 1994 at the cost of one octane unit, down to 96 research octane number (RON) from 97 RON.

As well as fuel price signalling to owners of older cars, as proposed in the 1993-94 Federal Budget, policymakers should be putting more pressure on refineries to maintain the high octane rating of super petrol other than by using lead. Extra processing at the refinery with the addition of octane enhancers such as MTBE (methyl tertiary butyl ether) or alcohols are methods now used in many countries for the replacement of lead and for controlling emission of carbon monoxide. They warrant more serious consideration in Australia.

Some concluding points

Although recent concern over lead has highlighted city children's exposure to lead in petrol, screening of blood lead in cities away from lead industries, especially in the last five years, has been meagre. A 1993 national review of current lead levels in children 27 has relied on very small samplings for its estimates of urban and suburban exposure. Furthermore, the latest Victorian results appear to contradict those studies. Clearly there is a need to determine more accurately the risk faced by the average urban child from lead in petrol.

Given that the Australian database on blood lead levels in children is quite inadequate, it would nevertheless be imprudent to take no action over lead in petrol. Scientists now agree that commonly occurring blood lead levels, and in particular those above ten micrograms per decilitre, incur a handicap in children's physical and mental development. As lead in food declines with the continued phasing out of soldered cans, lead from petrol is likely to become the largest source of blood lead if this is not the case already.

As well as the option of pricing leaded fuel somewhat higher than low-octane unleaded fuel to discourage its use, thought needs to be given as to how a reasonably priced high-octane low-lead fuel might be made available over the next fifteen years or so. Addition of oxygenates such as MTBE and alcohols and/or more refinery-based upgrading would reduce air pollution besides maintaining high octane levels for older cars.


1 Needleman, H.L.(ed). Human Lead Exposure. CRC Press, 1991: 25-27.

2 Alperstein, G., Reznik, R.B. and Duggin, G.G. 'Lead: subtle forms and new modes of poisoning'. Med. J. Aust., vol.155, 16 Sept. 1991: 407-409.

3 ibid.

4 ibid.

5 McMichael, A.J., Baghurst, P.A., Robertson, E.F., Vimpani, G.V. and Wigg, N.R. 'The Port Pirie Short Study. Blood lead concentrations in early childhood.' Med.J.Aust., vol. 143, 25 Nov. 1985: 499-503.

6 'Blood lead levels in Pt Pirie children'. South Australian Health Commission, Epidemiology Branch, Jan 1983.

7 Young, A., Bryant, E., Axford-Brooks, J., et al. 'Report on the Wollongong Lead Study, Wollongong.' University of Wollongong, 1990: 28.

8 Wright, B. ' Measuring the impact of lead'. Ecos,vol. 71, Autumn 1992: 25-27.

9 Edwards-Bert, P., Calder, I.C. and Maynard, E.J. 'National Review of public exposure to lead in Australia'. South Australian Health Commission, 1993.

10 Date, M. 'Tests find too much lead in children' The Sydney Morning Herald, 24 Sept. 1992.

11 Edwards-Bert, P., Calder, I.C. and Maynard, E.J. op. cit.

12 Berry, M. and Garrard, J. 'Revising Australian Guidelines for lead -an assessment of impacts'. Interim Report, NHMRC National Centre for Health Program Evaluation, May 1993.

13 'Air emission inventories (1985) for Australian capital cities'. Australian Environment Council, 1988.

14 Rutter, M. and Jones, R.R. (eds). Lead versus health. John Wiley and Sons, 1983: 156.

15 Rutter, M. and Jones, R.R. (eds) op. cit.

16 ibid.

17 Alperstein, G., Reznik, R.B. and Duggin, G.G. op. cit.

18 Eisinger, J. 'Our daily lead'. Nature, vol. 322, 14 Aug. 1986:601.

19 Reference 1, p.8.

20 Needleman, H.L., Gunnoe, C., Leviton, A., et al. 'Deficits in psychological and classroom performance of children with elevated dentine lead levels'. N. Engl. J.Med., vol. 300, 1979: 689-695.

21 Needleman, H.L., Schell, A., Bellinger, D., et al. 'The long-term effects of exposure to low doses of lead in childhood: an 11-year follow-up report'. N. Engl. J. Med., vol. 322, 1990: 83-88.

22 Bower, B. 'Lead in utero: low-level danger'. Science News, vol.131, 2 May 1987: 277.

23 McMichael, A.J., Baghurst, P.A., Robertson, E.F., Vimpani, G.V. and Wigg, N.R. op. cit.

McMichael, A.J., Baghurst, P.A., Wigg, N.R., Vimpani, G.V., Robertson, E.F. and Roberts, R.J. 'Port Pirie Cohort Study: environmental exposure to lead and childrens abilities at the age of four years'. N. Engl. J. Med., vol.319, 1988: 468-475.

Wright, B. op. cit.

Baghurst, P.A., McMichael, A.J., Wigg, N.R., Vimpani, G.V., Robertston, E.F., Roberts, R.J. and Tong, S. 'Environmental exposure to lead and children's intelligence at the age of seven years. The Port Pirie Study'. N. Engl. J. Med., vol.327, 1992: 9-11.

24 Gulson, B.J. 'Lead and the unborn child'. Paper presented to the 62nd ANZAAS Congress, Perth, 30 Sept. 1993.

25 Anon. 'Health effects of lead : current status'. Toxic, Nov. 1992: 9-11.

26 Edwards-Bert, P., Calder, I.C. and Maynard, E.J. op. cit.

27 Edwards - Bert, P., Calder, I.C. and Maynard, E.J. op. cit.

The author wishes to acknowledge the assistance of Rosemary Polya in the collection of resource materials for this paper and Karen Day for the formatting.

ISSN 1038-0116

Copyright Commonwealth of Australia 1993

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Published by the Department of the Parliamentary Library, 1993