PART 1: INTRODUCTION AND OVERVIEW PART 2: THE POTENTIAL EFFECTS OF HUMAN CONTAMINATION PART 3: CONTAMINANTS IN HUMAN BODY FAT PART 4: CONTAMINANTS IN BREAST MILK PART 5: LEVELS OF CONTAMINANTS IN UK BREAST MILK PART 6: MAIN CONCLUSIONS AND RECOMMENDATIONS REFERENCES APPENDIX: TOXIC PROPERTIES OF SOME CONTAMINANTS GLOSSARY OF TERMS AND ABBREVIATIONS UNITS
A report by Gwynne Lyons for WWF-UK
For further information contact:
Elizabeth Salter - Head, Toxics Programme
Surrey, GU7 1XR
UKTel: +44 (0)1483 412 518
Fax: +44 (0)1483 426 409
PART 1: INTRODUCTION AND OVERVIEW The post-war chemical revolution has resulted in global contamination. Thousands of substances have been released into the environment with few prior checks on their potential for causing long term harm. For many years, little attention was paid to what happened to these substances after they were released. However, it has now been realised that many are persistent and can cause unwanted effects in the longer term. Sometimes it is the parent molecule itself which is particularly hazardous, while in other cases, it can be a degradation product or a metabolite which is more harmful. This document highlights the particular concerns about fat soluble pollutants that are not readily broken down by metabolic processes, because these substances can be stored in body fats and build up to dangerous levels.
Predator birds, reptiles and mammals, including man, are particularly at risk, because persistent organic contaminants, along with some heavy metals, can build up in the food chain (bioaccumulate). Moreover, many of these pollutants can be passed on to offspring, either via the egg or via the placenta, at a particularly sensitive stage of their development. Mammalian offspring are potentially most at risk because further exposure to the pollutants stored in body fats occurs during breast feeding. Exposure of the foetus is related to the maternal body burden and, similarly, the exposure of a breast milk fed baby is related to the levels in a mothers adipose (fat) tissue.
Human exposure arises not only from the build up of environmental contaminants in the food chain and from exposure to contaminants in air and drinking water, but also from the direct ingestion of substances used in food packaging and in processed foods, and from the absorption through the skin of certain substances used in cosmetics. This report identifies many of the contaminants which have been found in human adipose (fat) tissue and breast milk.
The human race is now contaminated with hundreds of synthetic chemicals which would not have been found in our Victorian ancestors. Protecting our children from the legacy of these chemicals is a major challenge to modern society. Indeed, it is now recognised that the foetus can be damaged by relatively low levels of contaminants which do not affect the adult. Exposure in the womb can cause birth defects and affect our childrens future ability to reproduce and their susceptibility to diseases, including cancer. Functional deficits can also be caused, such that some children may not reach their full potential. Put simple, the integrity of the next generation is at stake.
As evidence of the harmful effects of these substances has grown, the need for international agreements to reduce or eliminate discharges and losses of a dozen or so of the most persistent and toxic substances has been recognised by the United Nations.1 However, because of their persistence, it will take many years for the risks from these substances to be eliminated. In addition, as the number of man-made chemicals has increased dramatically, there is still a threat from the numerous hazardous substances that remain in widespread use.
The global expansion of the organic chemical industry has been phenomenal, with total production in the 1950s estimated at around 7 million tonnes, compared to over 250 million tonnes in the early 1990s (CEC,1992). Not only the sheer volume of chemicals used, but also the number of chemicals, have increased dramatically, with perhaps around 80,000 chemicals currently in widespread use. This rapid post-war expansion in the chemical industry has certainly resulted in increased foetal exposure to many lipophilic contaminants. However, the problems associated with early-life exposure to pollutants are only now becoming a focus of attention. Rather like a snowball gathering snow as it is rolled along, mothers will pass a proportion of their contamination onto their children, who will then pick up more contamination from their own lifetimes exposure to numerous chemicals. DDT was first found in breast milk in 1950 (Laug et al.,1950), and PCBs were detected some twenty years later (Westoo and Noren; Acker and Schulte,1970). Nowadays, there is widespread contamination of mothers milk both in industrial cities, and in remote areas of the globe. Unfortunately, it has however taken many years for mankind to realise the extent to which we have contaminated our own species, and the susceptibility of developing offspring.
In humanitys rush to industrialise, wildlife throughout the world has been contaminated. Many species, including whales, seals, otters, alligators, birds and fish, have been adversely affected. However, because we are now living with so many pollutants, it is almost impossible to use field studies or epidemiological studies to ascertain which pollutants are responsible for causing which effects. This means that polluters are relatively safe from having to bear liability for perpetrating this mass chemical trespass of our bodies. Indeed, blame can only be established when pollutants cause rather specific effects, and there are clearly defined exposed and non-exposed populations, as was the case with asbestos and asbestosis and mesothelioma, and cigarettes and lung cancer. And even then, getting compensation in the courts is problematic, to say the least.
There are three overriding conclusions of this report. Firstly, over 350 contaminants have, at some time, been found in human breast milk. However, despite this, mothers should certainly not be discouraged from breast feeding. Secondly, urgent action should be taken to reduce foetal and neonatal exposure to man-made chemicals. And thirdly, substances that are persistent and able to bioaccumulate should be phased-out irrespective of their currently known toxicity, because if effects due to these substances do become evident, then it will be impossible to remedy these in the short term.
Part 2 of this report outlines the potential effects of exposure to chemical toxicants. Part 3 lists some substances and the levels that have been found in human body fats, while Part 4 identifies substances which have been detected in breast milk, and provides an indication of some of the higher concentrations that have been recorded. Part 5 looks at some of the levels of contaminants reported in breast milk from mothers living in Britain and outlines some future studies that Government departments are to oversee in the UK. Part 6 details the main conclusions of the report and makes some recommendations.
The toxic properties associated with the hundreds of chemicals that have been found contaminating the human species are numerous, and for a few of the compounds identified, some of these properties are briefly outlined in Appendix 1.
PART 2: THE POTENTIAL EFFECTS OF CONTAMINATION IN HUMANS
The foetus is particularly vulnerable to environmental toxicants, as is, to probably a slightly lesser extent, the neonate and the infant. This is because they have a greater relative exposure per kilogram of body weight and they have increased absorption and retention as their metabolism is less developed. Also, they are at a more sensitive stage of development because their cells are growing and changing rapidly, and in the foetus there is a high rate of cell production and cell division.
Given the known benefits of breast feeding, it is stressed that this report does not advocate that babies should not be breast fed. This is because breast feeding undoubtedly provides immunological and psychological advantages, and human milk is the ideal nutrient for infants. The alternative of powdered bottled milk formula may anyway also be contaminated with various pollutants. Indeed, chemicals such as phthalates, some of which possess endocrine disrupting properties, have been found in UK samples of infant formulae (MAFF,1996; FAC,1997). It should also be recognised that the foetus is likely to be far more sensitive than the neonate, and little can be done to avert transplacental exposure during this period if the mother is already contaminated. This report therefore reiterates the conclusion of expert committees, that on the basis of available information, the benefits of breast feeding outweigh the possible risks from chemical contaminants present in human milk.
With regard to the toxic substances in breast milk, first born infants may be at a higher risk than subsequent children, because mothers tend to excrete the largest proportion of their body burden of contaminants during their first lactation (Vaz et al.,1993). Premature and low birth weight infants may also be particularly at risk because they have less adipose tissue for the storage of lipophilic chemicals, which may mean that these chemicals are present at higher concentrations in vital organs. Heavy metals, such as lead and mercury, which may also be found in breast milk, may accumulate at different rates in the brain of premature infants (Jensen and Slorach,1991).
The potential effects of exposure to the chemicals which are now found as contaminants in human body fat and breast milk are numerous. Some of the contaminants identified are known to have the ability to cause cancer and some are able to impair the immune system. Others, termed hormone disruptors or endocrine disrupting chemicals (EDCs), are known to interfere with the normal functioning of the bodies own hormones, or chemical messengers. It is certainly particularly worrying that animal experiments show that if early life forms are exposed to hormone disrupting substances, when they are being programmed to control and respond to the hormone signals throughout life, then a whole series of irreversible effects can occur. For example, in utero exposure to sex hormone disrupting substances can particularly compromise the ability of that offspring to reproduce later in life, while exposure to other hormone disrupting substances, such as thyroid hormone disruptors, can de-rail normal brain function. Animal experiments have shown that exposure to low doses of numerous environmental toxic agents, during the neonatal period of rapid brain growth (or brain growth spurt), can lead to disruption of adult brain function and increase the susceptibility to toxic agents in later life. In humans, this period of rapid brain growth starts during the third trimester of pregnancy and continues throughout the first two years of life (Eriksson et al.,1998).
With regard to effects on infants, exposure to hormone disrupting substances in utero has been suggested to increase the incidence of birth defects of the reproductive tract (Kallen et al.,1986; Ansell et al.,1992; Nurminen et al.,1995; Garcia-Rodriguez,1996; Weidner et al.,1998), affect birth height (Dewailly et al.,1993) affect visual recognition and offspring intelligence (Jacobson and Jacobson,1996), and affect the sex ratio of babies born into a population (Moller,1996; Karin,1997). Furthermore, relatively high levels of some organochlorines have been associated with premature delivery (Saxena et al.,1980; Wassermann et al., 1982; Taylor et al.,1989; Fein et al., 1984), stillborn infants (Curley et al.,1969) and shortened lactation (Rogan et al.,1987; Gladen and Rogan,1995).
In women, exposure is implicated in effects such as endometriosis (Rier et al.,1995; Johnson et al.,1997) and increased breast cancer rates. However, the studies correlating the levels of organochlorine oestrogenic pollutants in human tissue with breast cancer incidence have been contradictory (Wolff et al.,1993; Adami et al.,1995; Hunter et al.,1997; Hoyer et al.,1998; see review in Lopez-Carillo et al.,1996), although none of the studies has looked at exposures in the womb and tried to correlate these with future breast cancer risk. It is, nevertheless, a reasonable hypothesis that man-made oestrogen mimicking compounds may be in part to blame for breast cancer. This is because it is well known that increased exposure to endogenous natural oestrogen, as occurs in women with early menarche, lack of breast feeding and late menopause, increases the risk of breast cancer (Henderson et al.,1988). Furthermore, recent studies have suggested that tamoxifen, an anti-oestrogenic pharmaceutical, can prevent breast cancer (BMJ, 23 May 1998). In addition, it may be that other man-made chemicals, apart from oestrogen mimicking compounds, are also partly to blame for the increased incidence of breast cancer. Some workers have found aromatic amines in breast milk and believe that these may play a role in the etiology of human breast cancer (deBruin et al.,1999).
With regard to effects on the testes, there is epidemiological evidence linking certain occupational exposures with increased risk of testicular cancer (Hardell et al.,1997). In addition, other small epidemiological studies also point to chemicals exerting effects on testicular function. Indeed, men who farm without pesticides or who eat food grown without pesticides have been found to have higher sperm concentrations (Kold Jensen et al.,1996; Abell et al.,1994). Fertility may also be affected. For example, in fruit growers, exposure to pesticides has been linked with an increase in time to pregnancy (see Health Council of the Netherlands,1997), although not all studies have shown effects on male fecundability (Larsen et al.,1998).
Decreased sperm counts have been found in men exposed in the womb to the synthetic oestrogen DES (diethylstilboestrol), as some years ago, DES was unfortunately used as a pharmaceutical medicament (Stillman,1982). This effect of oestrogen mimicking compounds is borne out by laboratory experiments on pregnant animals which show that other oestrogenic chemicals can also affect an offsprings sperm counts and sex linked behaviour traits (vom Saal et al.,1995). It is therefore a matter of considerable concern that human babies are now exposed in the womb to numerous oestrogenic pollutants which are contaminants of their mothers. The origin of testicular cancer may also be in foetal life. For example, there is some suggestion that testicular cancer and sperm count deficits may have a common cause (Moller and Skakkebaek,1999). Therefore, it is likely that exposure to some of these substances in the womb may make our children more predisposed to certain behaviours and certain diseases, including cancers in later life.
It is certainly a matter of increasing international concern that, in many industrialised countries, the incidence of hormone related cancers, such as breast cancer, prostate cancer, and testicular cancer, have all increased dramatically over the last 50 years. There are also good data to show, at least in certain areas, an increase in birth defects of the reproductive tract, and a decline in sperm counts. Moreover, there may be in-utero and neonatal exposure to other carcinogenic substances apart from endocrine disrupting substances. It is speculated that such exposures might be implicated in the rising levels of childhood cancers, although many factors are also likely to play a part, including genetic susceptibility. Given that in the USA, childhood cancer rates appear to be increasing at the rate of approximately 1% each year (EHP, January 1998), this report argues that it would be wise to endeavour to urgently reduce in-utero exposures to substances identified as possible carcinogens.
In the general population it may be that exposure to numerous substances with additive or even possibly synergistic effects are tipping certain people over the threshold for effects, but it may be that, for some substances, there is no threshold below which effects do not occur. In addition, it is likely that there are narrow sensitive windows of exposure when certain processes are at risk, although as central nervous system (CNS) development takes place over a relatively long time period, it is likely that offspring are particularly at risk of exhibiting effects on behaviour.
People and animals living in heavily industrialised areas and consuming polluted fish at the top of the food web, such as trout and salmon, are likely to be most at risk. For example, at least 14 species of fish and fish-eating wildlife in the Great Lakes have experienced effects, including population declines and reproductive problems, which have been attributed to persistent chemical contaminants (Health Canada,1997). In an effort to confirm the effects of simultaneous exposure to all the chemicals contaminants found in these Great Lakes fish, separate studies were undertaken. Scientists fed these contaminated fish to numerous species, including rats, coho salmon, ranch mink, and chickens, and in each case there were measurable changes in functionality or survivability (Villeneuve et al.,1981; Leatherland and Stonstegard,1982; Heaton et al.,1991; Daly et al.,1989; Summer et al.,1991). It is therefore perhaps not surprising that several studies have indicated effects on behaviour and neuromuscular development in the offspring of fish-eating women living in the Great Lakes area.
In one particular study, intellectual impairment was correlated to prenatal exposure to PCBs and co-contaminants. Furthermore, this study highlighted that exposure to contaminants in the womb appeared to be far more important than post natal exposure from breast milk. The Jacobsons' found that women who ate contaminated fish (from Lake Michigan), for 6 years prior to pregnancy, produced babies with poorer visual recognition as compared to less exposed children (Jacobson et al.,1985). At age four, the children who had had the higher cord serum PCB levels were associated with poorer verbal and memory performance and slower information processing. Even at 11 years old, the most highly exposed children showed lower full scale and verbal IQ scores (Jacobson and Jacobson, 1997). The Jacobsons' study suggested that exposure to contaminants in the fish was linked to an increase in the proportion of children at the lower end of the normal IQ range, although there was no evidence of gross intellectual impairment. This is important, because it highlights that only very detailed studies would pick up such effects.
A study in Mexico has also provided some startling comparisons in childrens development. This study suggested that compared to children with minimal pesticide exposure, children living in an area with heavy pesticide use, had decreased physical stamina, reduced memory, and amongst other effects, a reduced ability to draw a person, which was a test used to provide a non-verbal measure of cognitive ability. This study did not attempt to elucidate actual exposures, but nevertheless suggests that man-made chemicals may be causing alarming effects (Guillette et al.,1998).
Studies in Europe have also highlighted effects. For example, a study undertaken in the Netherlands, has associated pre and postnatal exposure to PCBs, dioxins and furans, to delays in psychomotor development in children (Koopman-Esseboom et al.,1996).
It could certainly be argued that more research is needed into the effects of pollutants on behaviour and brain function. For example, many environmental pollutants can alter thyroid function and it is known that the hormones secreted by this gland help coordinate the sequence of steps required for normal brain function (Porterfield,1994). Pollutants may therefore cause numerous effects, including, for example, the loss of ability to concentrate and to cope with stressful situations (Daly,1992; Lonky et al.,1996).
International agencies have already reacted to the warning bells. In June 1998, the World Health Organisation (WHO) reduced the tolerable daily intake (TDI) for dioxin like substances (which includes certain PCBs) to 1-4 picograms per kilogram body weight per day (pg/kg bw/day) from a previous level of 10pg/kg bw/day. This was in response to recent studies which had highlighted dioxins effects on neurological development and on the endocrine system. The WHO noted that subtle effects may already occur in the general population in developed countries at current background levels of 2-6 picograms/kilogram body weight (WHO, Press Release, 3rd June 1998). It is also rather alarming to note that in the industrialised world, the new TDI would be far exceeded by many babies during breast feeding (see Parts 4 and 5). In the UK, for example, the latest breast milk study, in 1993-94, found intakes of two month old babies were around 170 pg TEQ/kg bw/day which dropped to around 39 pg TEQ/kg bw/day at 10 months (MAFF, June 1997). These data show that 2 month old infants receive around 40 times in excess of the WHO tolerable daily intake, while 10 month old infants receive10 times in excess of the new WHO TDI. As of March 1999, the UK Government had still not reduced its TDI of 10pg/kg bw/day, and therefore had not come into line with the new WHO limits, but even these higher limits can be seen to be widely exceeded by breast fed infants.
BOX 2.0: SUMMARY OF THE POSSIBLE EFFECTS OF EXPOSURE TO ENDOCRINE DISRUPTING SUBSTANCES (Taken from Health Council of the Netherlands,1997)
The possible effects of in utero exposure to endocrine disruptors include:-
Abnormal development of the reproductive system, such as undescended testes and defects (hypospadias and epispadias) of the penis. Feminisation of the reproductive tract in males and masculinisation in females. Testicular cancer, and clear-cell carcinoma of the cervix or vagina. Decrease in sperm concentration and quality, and decrease in spermatogenesis.
Abnormal development of the central nervous system, leading to neurological, cognitive, and behavioural disorders (including effects on sexual behaviour), smaller head size at birth.
Other general developmental abnormalities, such as shorter pregnancies, lower birth weight, disturbed hormonal regulation or thyroid gland effects, arrested growth and effects on sex ratios.
The possible effects of exposure later in life include:-
Abnormal functioning of the reproductive system, and disturbance of hormonal regulation. In men, this could mean impotence and loss of libido, reduced testes size and weight, decreased sperm quantity and quality and altered spermatogenesis. In females, problems with breast feeding, menstrual or menopausal problems, endometriosis, alteration in fertility and an increased rate of abortions.
An increased incidence of cancers related to hormonal disturbance, such as breast, endometrial, prostate, testicular, ovarian, adrenal and thyroid cancers.
In a few cases, mostly due to industrial exposure, contaminants in breast milk have been implicated in causing demonstrable effects on infants in the short term. These have included perchlorethylene from a dry cleaning facility causing jaundice in the infant, and styrene exposure in a plastics factory, where several cases of inhibition of lactation were reported (Jensen and Slorach,1991).
Accidents have also provided evidence of the harmful effects of chemicals transferred in breast milk, and a particularly tragic event happened in Turkey in the 1950s, where about 4000 people were poisoned and about 500 died due to eating bread baked with flour made from HCB-treated wheat. Many of the children under two years old, who had been breast fed by mothers who had eaten the bread, died of a condition known as pink sore.
Other cases of mass accidental poisonings have occurred. In Japan, in the 1960s, there was an incident due to PCB contaminated rice oil, and a similar incident happened in Taiwan some ten years later. In Japan, the disease Yusho, characterised by skin abnormalities including chloracne, was reported in babies exposed in utero and in babies exposed solely through breast milk (Jensen and Slorach,1991, citing Yoshimura T.,1974).
Similarly, high levels of the related compounds, PBBs, were detected in Michigan residents in the early 1970s when these substances were accidentally included in animal feed. Exposed 2-4 year old children showed an inverse relationship between body burdens and developmental abilities, but it was not specified whether these body burdens were acquired in utero or from breast feeding (Jensen and Slorach,1991). The mercury poisoning incidents at Minimata in Japan in the 1960s, and in Iraq in the 1970s, are also well documented. In the later case, breast milk with around 200 ppb of mercury in whole milk was reported to be directly toxic to the infant (Jensen, 1996).
Maternal exposure to alcohol and tobacco in pregnancy are now well known to cause foetal alcohol syndrome and reduced birth weight. Similarly, in-utero marijuana exposure is reported to cause reduced body weight and head size, as well as reduced memory and verbal skills in infants and children (Nahas,1979). Other drugs are also known to cause unwanted effects in offspring, and so perhaps it should not be surprising that pollutants stored in our body fat may play a damaging role in our children's development. This is an issue which must be addressed, because even small shifts in behaviour and IQs at the population level, could cause profound economic and social consequences.