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Chemical Pollution and Mother's Milk

Chemicals: Hexachlorobenzene

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Hexachlorobenzene (HCB) is a persistent organochlorine chemical that is both a pesticide and an industrial byproduct. Its main use is as a fungicide on seed grains, including wheat, barley, oats, and rye.[1, 2] It also occurs as an impurity in other fungicides at low levels.[1] It had other uses in the past, including as a disinfectant in soaps.

HCB is formed as an industrial byproduct in chlorination processes, such as wastewater treatment. It also forms as a byproduct in the manufacturing and production of the wood preservative pentachlorophenol, of such chlorinated solvents as perchloroethylene and carbon tetrachloride, and of various pesticides.[1, 2]

HCB in the Body

Hexachlorobenzene can contaminate air, soil, grass, and food. Once it enters the environment, it breaks down very slowly, making it extremely persistent.

One reason for its slow breakdown, is that it does not dissolve well in water. It tends to stick very strongly to soil particles as well as to sediment on the bottom of lakes and rivers. It can also build up in wheat, grasses, some vegetables, and other plants when it is present in soil.[3] Soil contamination by HCB has occurred as a result of the improper disposal of HCB-containing industrial waste (often referred to as "hex waste").[2]

Because of HCB's persistence in soil and water, humans can be exposed to it in a number of ways. The major route of human exposure is through food: eating low levels from food produced in contaminated soil, eating contaminated fish, and drinking milk or eating dairy products or meat from cattle that grazed on contaminated pastures.[3] Other, less common, routes of human exposure to HCB include drinking contaminated water, breathing low levels in contaminated air, eating or touching contaminated soil, and working at a factory or in an industry that produces HCB as an unintentional byproduct.[3]

In Europe, the importance of diet as an exposure pathway was shown in a circumstance where livestock were fed HCB-treated grain. The meat and meat products made from the exposed cattle and pigs were contaminated with HCB.[2] A similar incident occurred in the United States in the mid-1970s in an industrial area of Louisiana, when cattle were quarantined because of especially high levels of HCB in their milk and fat. The cattle were exposed because the soil and grass they ate were contaminated from the disposal of hex wastes.[2]

HCB can be eliminated from the human body in urine, feces, and breast milk. HCB may also be transferred to the fetus across the placenta during pregnancy.[2] Levels of HCB in women have been found to decrease with each successive breast-fed child and with increased breastfeeding time.[1]

Controlling Exposures: Bans and Restrictions

Many countries have restricted the use of HCB as a pesticide, but its occurrence as an industrial byproduct is less strictly controlled.

The table below is a partial list of countries that have taken steps to reduce the use of hexachlorobenzene. Listing a chemical as banned or restricted does not guarantee that all use has truly stopped. Often considerable time passes before a country fully enforces a ban, sometimes because companies are allowed to use up their stockpiles of the chemical, and sometimes because of weak government enforcement. Also, countries sometimes permit chemicals that are otherwise banned to be used for special purposes.

Countries where the intentional use of Hexachlorobenzene has been banned or severely restricted[4]
Austria, Belgium, Czech Republic, Denmark, Germany, Hungary, Liechtenstein, Netherlands, Panama, Russia, Switzerland, Turkey, United Kingdom, and Yugoslavia.

HCB has not been used for commercial purposes in the United States since 1965. It has been listed as a pollutant of concern to the EPA's Great Waters Program because of its persistence in the environment, its potential to bioaccumulate, and its toxicity to humans and the environment.[5]

Assessing the Extent of Exposure: Limits and Benchmarks

Most chemicals that are either in widespread use or that have caused widespread contamination are subject to national and international benchmark levels, established to protect public health. But different agencies may have markedly different levels they consider "safe." These differences usually reflect the agencies' varying perspectives, as well as the kind of data they reviewed in setting levels. Conclusive evidence demonstrating that any one of these benchmarks is protective or superior to the others does not exist.

The Canadian Health Protection Branch has set a tolerable daily intake (TDI) level of 0.27 micrograms per kilogram per day (µg/kg/day).[6] Infant consumption of breast milk with average detected levels of HCB can frequently surpass this benchmark. The U.S. EPA has set a maximum contaminant level (MCL) of one part per billion (ppb) in drinking water.

Breast-milk monitoring Studies Measuring Hexachlorobenzene

Studies looking at HCB in breast milk have been conducted in the following countries:

AustriaGreeceNew ZealandTurkey
BelgiumHungaryNigeriaUnited Kingdom
CanadaIsraelNorwayUnited States
Czech RepublicItalyPolandUkraine
LuxembourgSweden France

Data from these studies are not all complete, however. In addition, countries not on this list may also have detectable levels of HCB residues in breast milk, since the list reflects only those areas where studies have been conducted, not just where HCB is measurable. The following section discusses issues that make it difficult to interpret the data.

Limitations of Studies Measuring Hexachlorobenzene

It is often difficult to draw conclusions about national and international trends in HCB contamination because of the many factors affecting measured levels, and because of limitations in the way data are reported. Some of these challenges include:

  • Absence of standardized methodology. No accepted and standardized method for conducting breast-milk monitoring studies has been established. Thus, differences may arise in the sampling time - when the breast milk is collected, or in the birth histories of the mothers - women who have breast-fed multiple children might be mixed in with women who are breastfeeding for the first time.

  • Distinct regional differences in HCB use and contamination. HCB is both an agricultural pesticide and an industrial byproduct, so its concentration in a given area depends on what is produced or grown in that area. Therefore, national averages may obscure the different exposure scenarios in the various regions of a given country.

  • Few studies. Many countries do not have multiple studies over time. Instead, the information on HCB residues may be just a snapshot of a particular time. Where that is the case, it is difficult to generalize about how the conditions in a country may have changed over time.

  • Small study populations. Because of the cost and time involved, many studies measuring HCB levels in breast milk test only a few people. In instances where the only data on a country's HCB exposure levels are from studies with small sample sizes, it is difficult to draw reliable conclusions about the entire population's exposure.

  • Bias. The selection of study participants often presents challenges. In many studies, women may have been chosen to participate based on potentially high exposure to the chemical of interest, thereby driving average values from the study higher.

Some Important Examples of Hexachlorobenzene in Breast Milk

Several useful studies on hexachlorobenzene are available.

HCB has been detected in breast milk around the world. It is also commonly found in other fatty tissues.[7, 8] Historically, women in areas with less industrialization have had significantly lower levels of HCB in their breast milk. For instance, average HCB levels detected in breast milk in Kenya in the mid-1980s were just 1/100th of average levels found in Sweden and Germany at a similar time.[9]

HCB levels in breast milk have declined in some countries over the past two decades, probably the result of changes in fungicide use and procedural improvements in industry that have resulted in a reduction in the production of HCB byproducts.

Unique Exposure Situations: Diet and Industrial Exposure

The most notorious example of breast-milk contamination by HCB occurred in Turkey in the 1950s. During a period when bread wheat was unavailable, HCB-treated seed wheat intended for agriculture was used for food. Between 1955 and 1959, 500 people were fatally poisoned by eating bread made with the contaminated seed. More than 4,000 people fell ill as a result of the exposure. Most of the sick were affected with a liver condition called porphyria cutanea tarda, which disturbs the metabolism of hemoglobin and results in skin lesions. The poisoning was often fatal for children. In some villages, almost all breastfeeding children under the age of two, whose mothers had eaten tainted bread, died. Locally, this condition was called "pembe yara" and probably resulted from high doses of HCB passed on through the breast milk. In one mother's breast milk during the incident, the HCB level was found to be 20 parts per million in lipid, approximately 2,000 times the average levels of contamination found in breast-milk samples around the world. [1, 2] Follow-up studies 20 to 30 years after the poisoning found average HCB levels in breast milk were still more than seven times the average for unexposed women in that part of the world,[10, 11] and 150 times the level allowed in cow's milk.[12]

Severe health effects from HCB exposure in breast milk are not common. In Turkey, the "pembe yara" outbreak occurred because of direct exposure to acutely poisonous levels. In most cases where HCB is detected in breast milk, the dose is far lower. However, the Turkey example illustrates the potential for dietary HCB exposure and lactational transfer.

The importance of dietary exposure to HCB has been demonstrated in many studies. In Germany, women who followed a healthy diet (low meat consumption and high vegetable and fruit intake) for at least three years had much lower levels of HCB in their breast milk. Conversely, women who ate more than 700 grams (1.5 pounds) of meat per week were found to have higher levels of HCB.[13]

HCB concentrations in breast milk differ depending on regional exposure patterns. For example, in France, breast milk from women who were recent Algerian immigrants contained three times as much HCB as native French women, suggesting a marked difference in their exposure early in life.[1]

In many countries, a clear difference emerges between HCB exposures in industrial and non-industrial areas. In the Czech Republic, higher levels of HCB in breast milk were found in industrial areas. These areas (Prague and Kladno) were home to a variety of industries that utilized combustion processes that emitted heightened levels of HCB.[14] A study in 1992 found that HCB levels in the breast milk of women living in the Kola Peninsula of Russia were twice as high as in Norway and the Netherlands.[15] This area also has much higher levels of industrial pollution than other parts of Europe.

Time Trends

Sweden has witnessed a clear decline in the levels of HCB detected in breast milk. Figure 21 illustrates this marked decrease. In 1980, HCB was withdrawn in Sweden from use as a fungicide. In addition, HCB's production as an industrial byproduct decreased with improvements in industrial technologies. The average concentrations found in breast milk varied in the 1970s, but scientists have measured a steady decline since the ban.[16]

Figure 21

Norway experienced a similar decrease, with levels of HCB in breast milk dropping by 65 percent between the mid-1970s and early 1990s. HCB was never used as a fungicide in Norway, so it is thought that the decreased levels are a result of improvements in industrial processes, especially in wood treatment.[17]

Figure 22 shows how HCB levels in breast milk have drastically decreased in the North Rhine Westphalia region of Germany.[18] Over the course of a decade, HCB levels in breast milk declined by more than 85 percent. Again, the decline may be a result of changes in fungicide use and improvements in various production practices.

Figure 22

Studies conducted in Belgium, Canada, Denmark, the Netherlands, and Switzerland suggest a decline in the HCB levels found in breast milk there also.[1]

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1. Jensen, A.A. and S.A. Slorach. Chemical Contaminants in Human Milk, 1991, Boca Raton Ann Arbor Boston: CRC Press, Inc.

2. Courtney, K.D. Hexachlorobenzene (HCB): A Review, Environmental Research 1979; 20: p. 225-266.

3. ATSDR. ToxFAQs for Hexachlorobenzene, 1997, ATSDR.

4. WWF. Summary of Where POPs are Being Used, Banned, or Restricted, 2000, World Wildlife Fund.

5. U.S. EPA. Deposition of Air Pollutants to the Great Waters, 1994, United States Environmental Protection Agency: Research Triangle Park, NC.

6. Craan, A.G. and D.A. Haines. Twenty-Five Years of Surveillance for Contaminants in Human Breast Milk, Archives of Environmental Contamination and Toxicology 1998; 35: p. 702-710.

7. Abbott, D.C., et al. Organochlorine Pesticide Residues in Human Fat in the United Kingdom 1976-77, British Medical Journal 1981; 283: p. 1425-1428.

8. Mes, J., D.J. Davies, and D. Turton. Polychlorinated Biphenyl and Other Chlorinated Hydrocarbon Residues in Adipose Tissue of Canadians, Environ Contam Toxicol 1982; 28: p. 97-104.

9. Kanja, L., et al. Organochlorine Pesticides in Human Milk from Different Areas of Kenya 1983-85, Journal of Toxicology and Environmental Health 1986; 19: p. 449-464.

10. Gocmen, A., et al. Hexachlorobenzene Episode in Turkey, Biomedical Environmental Science 1989; 2(1): p. 36-43.

11. Cripps, D.J., et al. Porphyria Turcica Due to Hexachlorobenzene: A 20 to 30 Year Follow-up Study on 204 Patients, British Journal of Dermatology 1984; 111(4): p. 413-422.

12. Peters, H.A., et al. Epidemiology of Hexachlorobenzene-induced Porphyria in Turkey: Clinical and Laboratory Follow-up After 25 Years, Archives of Neurology 1982; 39(12): p. 744-749.

13. Schade, G. and B. Heinzow. Organochlorine Pesticides and Polychlorinated Biphenyls in Human Milk of Mothers Living in Northern Germany: Current Extent of Contamination, Time Trend from 1986 to 1997 and Factors that Influence the Levels of Contamination, The Science of the Total Environment 1998; 215: p. 31-39.

14. Schoula, R., et al. Occurrence of Persistent Organochlorine Contaminants in Human Milk Collected in Several Regions of Czech Republic, Chemosphere 1996; 33(8): p. 1485-1494.

15. Polder, A., et al. Dioxins, PCBs and some Chlorinated Pesticides in Human Milk from the Kola Peninsula, Russia, Chemosphere 1998; 37(9-12): p. 1795-1806.

16. Noren, K. and D. Meironyte. Certain Organochlorine and Organobromine Contaminants in Swedish Human Milk in Perspective of Past 20-30 Years, Chemosphere 2000; 40: p. 1111-1123.

17. Johansen, H.R., et al. Congener-specific Determination of Polychlorinated Biphenyls and Organochlorine Pesticides in Human Milk from Norwegian Mothers Living in Oslo, Journal of Toxicology and Environmental Health 1994; 42: p. 157-71.

18. Furst, P., C. Furst, and K. Wilmers. Human Milk as a Bioindicator for Body Burden of PCDDs, PCDFs, Organochlorine Pesticides, and PCBs, Environmental Health Perspectives Journal 1994; 102: p. 187-93.

last revised 5.22.01

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