POSSIBLE HCB EMISSION from a MAGNESIUM EXTRACTION PLANT using ASBESTOS tailings.

Introduction

Two of the main emissions from Magnola's magnesium extraction plant that cause concerns are Hexachlorobenzene (HCB) and dioxins. Dioxin is a general term used to refer to all polychlorinated dibenzo-para-dioxin and dibenzofurans (PCDD/Fs) of which the most potent and extensively studied congener is 2,3,7,8-tetrachlorinated dibenzo-p-dioxin (2,3,7,8-TCDD).
Because the Comité de Citoyens expressed that the primary concern of residents around Magnola is the effect of HCB ) exposure on human health, it will be the emphasis of the health assessment.

HCB was widely used as a fungicide. Residents of Diyarbakir in southeastern Turkey consumed bread prepared from wheat treated with HCB between 1955 and 1961, and an outbreak of porphyria cutanea tarda (PCT) resulted. There were approximately 3000 patients who suffered in various degrees, and the victims were exposed to 50-200mg HCB/day for several months (Cam & Nigogosyan, 1963). It was the first major incident to demonstrate the danger of exposure to HCB. Since then, the general public has been and still is concerned about the exposure to HCB and other organochlorine compounds. This issue deserves attention because both HCB and dioxins accumulate in lipid-rich tissues of animals including humans (To-Figueras et al. 2000). Moreover, both HCB and dioxins are widely distributed. In particular, the long-distance transport and distribution of HCB via the troposphere is especially important and it makes HCB an evenly distributed semi-volatile organic compound around the world. Therefore, HCB emission has health and environmental implication at both local and global levels. Both HCB and dioxins are still being released into the environment as by-products of various industrial processes. In the United States over 4000 tons of HCB are generated annually as a waste byproduct mainly from the manufacture of chlorinated solvents (Michielsen et al. 1999). Waste incineration is another source of HCB and dioxins emission into the environment. In the magnesium extraction process, HCB and dioxins are the by-product of electrolysis.
However, there are some difficulties in our investigation. First, currently Magnola is not at its full operation capacity, and there is no real data to be collected and analyzed. Magnola's emission projection cannot be verified yet. In addition, there is little information on the effects of HCB exposure to certain subsets of population. Animal studies occasionally show species differences and when comparable human studies do not exist, it is somewhat difficult to interpret conflicting findings of animal studies.

Project Issue in a Broader Context / Literature Review

Potential Adverse Health Effects Caused by HCB and Dioxins
Except from the accidental contamination follow-up studies, there is little information available regarding the toxicity of HCB. In particular, knowledge of possible health effects due to chronic exposure to HCB is incomplete. However, HCB and dioxins share some common characteristics. Medical researchers are currently investigating the contribution of HCB exposure to the following five most observable health effects:
1. Porphyria cutanea tarda (PCT)
2. Increased risk of thyroid cancer and soft-tissue sarcoma
3. Liver dysfunction and liver cell tumors
4. Impaired immune system function
5. Adverse effects on reproduction

1. Porphyria cutanea tarda (PCT)
As mentioned previously, the HCB contaminated bread incident in Turkey demonstrated that an exposure to a large dose of HCB would cause PCT in humans. It should also be mentioned that researchers also believe an acute exposure to TCDD can trigger PCT in some individuals (Mukerjee 1998). More precisely, individuals who were exposed to either substance would develope type IV PCT. (Table 2).
Table 2: Types and descriptions of PCT (Modified from De Mola et al. 1996)
Porphyria type Description
I Sporadic; deficiency of the enzyme is only in the liver
II Hereditary; autosomal dominant transmission; enzymatic defect in all cells
III Hereditary porphyria with normal uroporphyrinogen-3-decarboxylase (URO-D) activity in red blood cells
IV Toxic form due to an exogenous chemical agent (e.g. HCB)

This disorder primarily affected children under 16 years of age; in the Turkish bread incident only 10% of the patients were over 16 years of age (Courtney 1979). The interval between HCB ingestion and the development of the initial symptoms of PCT is approximately 6 months (Cripps et al., 1984). In a normal individual, porphyrins are incorporated into hemoproteins. HCB-induced porphyria is characterized by a deficiency of the enzyme uroporphyrinogen decarboxylase resulting in the accumulation of excessive porphyrins in the liver and increased urinary excretion of highly carboxylated porphyrins (Michielsen et al. 1999). Urine samples from patients suffering from PCT were red or brown. Patients had visible skin lesions, experienced loss of appetite and were irritable with cholic. The acute symptoms became less frequent 5 years after exposure to HCB. However, there are other symptoms such as small stature, small hands and painless arthritis, which are considered permanent effects (Cripps et al. 1984).

2. Increased Risk of Cancer
Animal study experiments indicate that HCB is a rodent carcinogen (van Birgelen, 1998). The organs that appear to be the major targets of this substance are thyroid, parathyroid and adrenal glands and liver. An investigation of effects of HCB exposure on human health conducted in Flix, Spain reveals that all subjects who are cancer patients have been workers in an electrochemical plant for some time. This study will be discussed in detail later in the report. The finding suggests that although International Agency for Research on Cancer (IARC) currently designates HCB as a class 2B carcinogen (i.e. possible carcinogen), its carcinogenic potency should be reviewed. Regarding dioxins, the International Agency for Research on Cancer (IARC) evaluated 2,3,7,8-TCDD and classified it as a Group 1 substance, which means it is carcinogenic to humans. Overall, it was found that the carcinogenicity of TCDD was for all cancers combined rather than for any specific site (McGregor et al. 1998). However, there was inadequate evidence in humans for the carcinogenicity of all other PCDDs. With regard to PCDFs it was concluded that there is inadequate evidence in humans for carcinogenicity.

3. Liver Dysfunction
Liver is a major organ affected by the exposure to HCB. Only fat tissue has a higher HCB concentration than liver. In fact, porphyria can also be considered a liver disorder since the overproduction of porphyrins occurs in the liver of the affected individuals. Linear relationships exist between fat and blood HCB concentrations and between liver and blood concentrations. Den Tonkelaar et al. (1978) measured HCB concentrations in liver, kidney and brain tissues after 13 weeks of administration of HCB to pigs, and it was demonstrated that HCB concentration in liver is higher than that in kidney and brain. (Table 3)

Table 3: Mean HCB concentration in liver, kidney and brain of pigs that received HCB for 13 weeks (Modified from Den Tonkelaar et al. 1978)
HCB (mg/kg/day) HCB (mg/kg)
Liver Kidney Brain
0.5 3.3 2.17 1.95
5.0 42.3 17.9 19.9

Animal studies reveal that chronic exposure to HCB could induce liver cell tumors in rats, mice and hamsters. Furthermore, De Mola et al. (1996) reported that female PCT patients during pregnancy may have liver dysfunction.
Although a high dose of PCDD/F can cause liver damage in humans, effects of low level exposure are questionable (Triebig et al. 1998). While there is a notable 3-fold increase in liver cancer mortality based on a 22-year follow-up study in Japan, such a pattern was not found based on a 12-year follow-up study in Taiwan, where there is no increase in liver tumor incidence in the affected population (McGregor et al. 1998).

4. Immune System Impairment
The effects of HCB on the immune system are species-dependent. For instance, HCB stimulates the immune response in the rat (Vos 1986). In contrast, HCB seems to suppress humoral and cell-mediated immunity in the mouse (van Loveren et al. 1990). Despite the documented experimental effects of HCB on animals, there is no systematic study of the effects of HCB in the human immunological system (Queiroz et al. 1997).
Queiroz et al. (1997) investigated the health status of former workers in a chemical plant. Impairment in neutrophil migration was observed in the exposed workers when compared to subjects in the general population.
Although Michielsen et al. (1999) stated that the mechanism by which HCB affects immune system is still unclear, Queiroz (1997) suggested HCB is biotransformed to sulphur-containing metabolites originating from the conjugation to glutathione (GSH). GSH protects cells and tissues from free radicals, functions as a detoxifying agent and regenerates immune cells. Presence of GSH will stop the replication of many intracellular pathogens. Koss et al. (1987) demonstrated a depletion of GSH level after administration of HCB to rats. The impairment of neutrophil chemotaxis observed may be attributed, at least in part, to the HCB-induced decrease in GSH levels (Queiroz et al., 1997).
In another study, Queiroz et al. (1998) also found significantly greater levels of immunoglobulin G (IgG) and IgM in HCB exposed workers when compared to non-exposed subjects (Table 4).

Table 4: Mean serum IgG, IgM levels in control subjects and HCB-exposed workers
Control subjects Exposed workers
Mean serum IgG level (mg/ml) 13.75 17.50
Mean serum IgM level (mg/ml) 1.37 1.80

IgG and IgM levels of HCB-exposed workers are similar to those of alcoholic cirrhosis patients. Therefore, the changes in IgG and IgM levels support the indication of hepatic dysfunction in the HCB exposed workers. In animal studies, Wistar rats that were exposed to HCB also show a dose-response relationship for increase in total serum IgM, IgG and IgA levels (Michielsen et al., 1999).
It has been demonstrated that HCB has a stimulating effect on the number of B-lymphocytes, particularly the B1 subset, which is responsible for the production of 50% of total serum IgM. The derangement of the B1 cell population has been associated with human autoimmune diseases, which may be frequently associated with dermal lesions, especially in the sun-exposed areas. Some studies demonstrate that HCB induces the formation of autoantibodies and causes dermal lesions, suggesting that an autoimmune mechanism may underlie HCB induced symptoms.
Moreover, oral exposure to HCB for 6 weeks suppressed Natural Killer cell (NK) activity in rat lungs in a dose-related manner (van Loveren et al., 1990). In rats that were exposed to 450mg HCB/kg food, the NK activity in the lung was one-third of that of normal rats. NK activity combats neoplastic and virus-infected cells. This may explain why HCB exposure is thought to contribute to an increase in cancer risk and immune system impairment.
TCDD affects the immune system by affecting the B and T-lymphocytes. In in vitro studies, human B cells were reduced at TCDD concentrations as low as 10-14 mmol. The development of T cells in animals was also shown to be impaired by TCDD (Jung et al. 1998).

5. Adverse Effects on Reproduction
In animal studies, it was found that the male reproduction system was affected only by repeated exposure to very high doses of HCB (Den Tonkelaar et al., 1978). In contrast, female rhesus monkeys appear to be more sensitive since HCB exposure causes severe changes in ovarian structure. This seems plausible because males produce a large quantity of sperm continuously, whereas the number of oocytes in females is fixed and it is observed that the quality of the oocytes deteriorates as the females approach the end of the reproductive age. Exposure to HCB might accelerate the process of deterioration.
Certain dioxin congeners, for instance 2,3,4,7,8-PCDF, were reported to have reproductive effects such as lowering sperm count and alteration of female genital tracts. TCDD exposure has also been attributed to decreased sperm production (Mukerjee 1998).

Controversy over Effects of HCB and Dioxin Exposure

Although some attribute effects described above to the exposure to compounds such as HCB and dioxins, others do not agree. For instance, Safe (2000) states that the sperm counts have not decreased over the last 60 years in North America. In addition, there are studies that show the human immune system actually uses chlorine, bromine and iodine to kill invading microorganisms (Gribble, 1994). In addition, some studies of populations that are chronically exposed to HCB do not indicate adverse health effects. For instance, Burns and Miller (1975) did not find evidence of adverse health effects due to the exposure to HCB.

Research Question / Hypothesis

The previous section explained the possible adverse effects of exposure to HCB and dioxins on human health, and there are two main questions:
1. What are the routes of exposure?
2. What are the factors that will influence the susceptibility of different subsets of the population?

Methodology

Previous follow-up studies on the adverse health effects of accidental exposure to HCB and dioxins and the investigation of the health status of residents in communities where ambient HCB concentration is high are particularly useful. In addition, animal studies provide some insight to the action mechanisms of these compounds.

Analysis and Discussion

Routes of Exposure
Occupational Exposure:
The two main routes of occupational exposure are believed to be inhalation and dermal contact. Nevertheless, other factors and routes of exposure merit attention and further investigation because a study by Currier et al. (1980) found that the HCB level in blood of workers in chlorinated solvent production plant was strongly associated with the number of years worked in the plant, but was poorly correlated with environmental measurements such as work category or activities. The lack of correlation between HCB exposure and HCB blood concentration made the researchers suspect that the exposure was interrelated with other factors such as improper handling of foodstuff and poor personal hygiene. Queiroz et al. (1998) also noticed that the serum HCB level did not correlate with the length of exposure to the substance, which also supports the above explanation for the lack of dose-response relationship for workers who have been exposed to HCB.
Routes of Exposure for the General Population:
For the general population, the major source of HCB and dioxins exposure is as a contaminant in the diet (Michielsen et al., 1999; Mukerjee 1998). Since both accumulate in fat tissues, it is not surprising that they are detected in food items rich in fat, especially those of animal origin (van Birgelen, 1998). However, HCB can also be found in produces such as vegetables and legumes.
The mean HCB levels in US food during 1990-1991 were less than 1 ppb. An interesting note here is that HCB concentration in UK potato peel was found to be as high as 6 ppb (Wang & Jones 1994). World Health Organization estimated in 1997 that the daily intake of HCB by adults ranges from 0.0004 to 0.003 mg HCB/kg body weight. The total daily intake of PCDD/F in terms of total toxic equivalents (TEQ) is 115pg/person in the Netherlands. This figure should be higher in the United States since their daily intake of TCDD alone (34.8pg/person) is nearly twice that of an average Dutch citizen (20pg/person).
The general population exposure will also be from ambient air, contaminated drinking water and also through contact with contaminated soil.
Ballester et al. (2000) also found that although having a spouse who works in an electrochemical factory was associated with an elevated HCB concentration in serum, relatives other than spouses did not show any increase in HCB concentration in serum.

Populations in the Vicinity of Magnola
There are three towns in the vicinity of Magnola magnesium extraction plant: Asbestos (population 6700), Danville (1900) and Shipton (3000). Since the Asbestos mines reduced its operation in the 1980s, the surrounding communities have not been growing and they have the characteristics of an aging population. Magnola will be the only major industrial facility in that area, the other nearest industrial establishments are in Sherbrooke.

Susceptibility of the General Population
According to Sala et al., (1999) the exposure to HCB did not affect the general health status of a population over 14 years of age in Flix, Spain where the level of HCB in the air is 35ng/m3. This is approximately 100 to 1000 times higher than the readings obtained from other locations. The unusually high HCB level in the air attracts our attention and the possibility of a reading from a contaminated instrument, similar to the observation made by Basu et al. (2000), could not be ruled out. However, we cannot verify the validity of the air samples taken in Flix, Spain.
According to Magnola's estimates, the highest ambient air (i.e. air samples taken at the boundary of the facility) HCB level under all weather conditions will be approximately 1.4ng/m3, which is higher than the air HCB level from other locations . Again, since the sample reading from Flix, Spain is yet to be verified, the elevated air HCB level due to Magnola's emissions justifies the concerns of Comité de Citoyens.

The EPA estimates that, if a person were to inhale air containing HCB at 0.002g/m3 (2ng/m3) over their entire lifetime, that individual will theoretically have no more than a one millionth increased chance of developing cancer as a direct result of the chemical (EPA, 1993). Authors of the Environmental Report by EPA chose 2.2ng/m³ as the limit. If the air HCB level is in fact 35ng/m3 in Flix, Spain, where the general population of the community has not shown observable adverse health effects, the HCB emission from Magnola at 1.4ng/m3 appears acceptable. The study in Flix, Spain by Sala et al. (1999) is particularly useful because the study site is in a rural environment and the only industrial activity present is the electrochemical factory, which has been producing volatile chlorinated solvents in the last four decades. Furthermore, the concentrations of other airborne organochlorine compounds in the air of Flix, Spain are similar to that of the reference community. This lowers the possibility of the effect of other sources of organochlorine compounds. In addition, 1800 residents (43% of the population over 14 years of age) of that community were included in that study. This large sample size also allows us to use it as a model to predict the effect of HCB in the air for the residents near Magnola project.

Susceptibility of Individuals with High HCB and Dioxins Exposure
However, Sala et al. (1999) also pointed out that the most highly exposed subjects, males who worked at the electrochemical factory, have a significant increase of pathology related to HCB including goiter, hypothyroidism and cancer. It is important to note that according to Okamura et al. (1987), overt hypothyroidism is more common in women in a normal population. A higher than expected incidence of overt hypothyroidism in male workers would be an implication of adverse health effects due to HCB exposure. Exposure to dioxins was reported to have no effect on thyroid stimulating hormone level in recycling plant workers (Triebig et al. 1998). Grimalt et al. (1994) also found that thyroid and brain neoplasm and soft-tissue sarcomas in males in Flix, Spain are higher than expected. All males who had cancer in that study had worked in the factory, while none of the female subjects in that study worked in the electrochemical factory. This conclusion is supported by another more recent study by Herrero et al. (1999), who found the mean HCB level in serum is 72.8ng/ml for males, and 17.7ng/ml for females of Flix, Spain. This is much higher than the serum HCB level obtained from studies conducted at other locations.

Gender Differences
Grimalt et al. (1994) also mentioned the possibility of gender differences in the excretion of HCB derivatives. Burns and Miller (1975), found a higher HCB blood residues in males than in females. In that study there were 22 husband-wife pairs living in exposed households and males had higher residues (5.10ppb) than the females (1.70ppb). However, To-Figueras et al. (2000) believe that the most probable explanation for higher HCB concentration in blood samples from males is their employment in the electrochemical factory, which is the main determinant of the variation in HCB body burden. It is also important to point out that Ballester et al. (2000) also found that among non-factory workers, the HCB concentrations in blood were higher in women (14.3ng/ml) than in men (8.1ng/ml).
In fact, a study conducted by To-Figueras et al. (1997) indicated that pentachlorobenzenethiol (PCBT) is a good urinary marker of HCB internal dose, and by measuring the PCBT in urine samples, the researchers suggest that the HCB metabolism is probably more efficient in men than in women. This means that although males have a more efficient metabolism of HCB and eliminate more PCBT than females, due to the high exposure to the substance at work place, their HCB level in the serum is still much higher than women.
Regarding the effects on reproduction, it appears that female subjects are more susceptible than males. HCB is known to be a potent oocyte toxicant in primates. The primordial germ cell appears to be sensitive to HCB levels before the onset of porphyria. Initial analysis of serum HCB and risk for spontaneous abortion by Jarrell et al. (1998) showed that they were significantly associated. However, they concluded that risk of spontaneous abortion was not restricted to patients who experienced a clearly identified high exposure event. The induction of porphyria by HCB was not associated with serum HCB levels or adverse reproductive outcome when assessed at approximately 40 years after exposure of the contamination incident. It is also important to note that currently the women in the control group living in Ankara have a higher blood HCB level than the women who lived in Diyarbakir, where the contamination incident occurred in the 1950s. Moreover, the threshold for risk of spontaneous abortion was possibly in the range of HCB levels of control groups toward the end of their reproductive lifetime. Factors such as number of pregnancies, babies and abortions may play a role in determining body burden of lipophilic chemicals such as HCB (Jarrell et al. 1998).
Another complication in reproduction noted in female porphyria patients is the observation that hormonal changes during pregnancy precipitate the disorder (De Mola et al. 1996).

Infants
The most vulnerable individuals in the general population are the infants, particularly breast-fed newborns. There was a high mortality (>95%) among young children, especially those under the age of 1 year, who were exposed to HCB via placenta or maternal milk in the Turkish contamination incident (Michielsen et al., 1999). In fact virtually all children between the ages of 2 months and 5 years were eliminated in the affected communities (Courtney, 1979). One of the reasons why infants are particularly vulnerable is that they have not yet fully developed detoxification mechanisms and their organs are in the process of rapid growth. Moreover the developing immune system seems to be particularly vulnerable to the immunotoxic effects of HCB and dioxins (Michielsen et al. 1999; McGregor et al. 1998). Nakashima et al. (1997) found that a great portion of the HCB accumulated in dams during pregnancy was postnatally transferred to suckling pups through milk after birth. They concluded that prenatal transfer of HCB to rat fetuses was small, and a great portion of the HCB that accumulated in dams during pregnancy was postnatally transferred to suckling pups. Cross-fostering in animal studies also showed that normal pups that were fed by dams that had been exposed to HCB died within days after suckling from the HCB-exposed female (Courtney, 1979). Intakes of dioxins by breast-fed human babies can exceed the Tolerable Daily Intake (TDI) of 10pg/kg body wt/day by almost 20-fold. (Pollitt, 1999)
The above findings show that breast-fed babies are particularly vulnerable. Czaja et al. (1997) also indicated that lipophilic compounds such as HCB accumulate in human fat tissue and are excreted in human milk through lactation. Breast milk is rich in fat and the HCB concentration in the adipose tissue is about 50 times higher than maternal blood HCB concentration (Ando et al. 1985). Similarly, dioxins are lipophilic and are highly concentrated in the milk.
Mothers who consume more fat-rich items such as seal blubber and beluga skin have a higher amount of HCB in their body. This is observed in Inuit communities in the Arctic region (Dewailly et al., 1993). Traditional Inuit diet consists of fat-rich items, and Inuit women breast milk samples were found to have higher concentrations of HCB than breast milk samples from Caucasian women in southern Quebec. To eliminate the discrepancy caused by possible genetic differences in the two populations, populations of two Inuit communities were compared. While 89% Inuit from Hudson Straight region consumed fermented seal or beluga blubber once a year or more, only 28% of women from the Ungava reported the same habit. HCB concentrations in the Hudson Straight group and in the Ungava group were 188ng/g breast milk fat and 115ng/g breast milk fat respectively.

Variations in milk fat dioxin and HCB concentrations in samples from different countries may be in part explained by the differences in diet. Milk samples from developed countries have a higher dioxin TEQ than samples from undeveloped countries (Mukerjee 1998), which may be attributed to differences in meat consumption. Adverse Effect Threshold Level There is little information on the threshold levels and dose-response relationship of HCB and on HCB-related adverse effects in humans (To-Figueras et al., 2000). Animal tests indicate that the LD50 in mice and rats is 10 000mg/kg body weight, and this means that HCB has low to moderate acute toxicity from oral exposure (Courtney 1979). With regard to dioxins, a similar lack of dose-response relationships has been reported. In fact, with regard to quantitative cancer risk assessment for dioxins, the data collected by Becher et al. (1998), do not indicate the presence of a threshold level. The EPA has determined that there is not enough information to establish a Reference Concentration (RfC) for HCB but the Reference Dose (RfD) for HCB is 0.0008 mg/kg/d. (80mg/kg/d) The RfD is a reference point to gauge the potential effects. It is the estimated daily exposure level at which there will not be appreciable risk of deleterious effects even for the most sensitive individuals in their life-time. Exceeding the RfD does not imply that an adverse health effect would necessarily occur. As the amount and frequency of exposure exceeding the RfD increase, the probability of adverse health effects also increases. A comparable measure for dioxin related health effects is the TDI, 10pg/kg body weight/day, which is derived from the No Observed Adverse Effect Level (NOAEL) in animal studies with an added safety factor. Another difficulty is that the half-life of HCB in humans is still unknown (van Birgelen, 1998; WHO 1997), although Currier et al. (1980) suggested that the half-life of HCB in chemical plant workers appeared to be about 2 years. This seems reasonable since the half-life of HCB is reported to be 2.5-3 years in rhesus monkeys (Rozman et al. 1981). As mentioned previously, the World Health Organization estimated (1997) that the daily intake of HCB by adults ranges from 0.0004 to 0.003 mg HCB/kg body weight, while the RfD is 80mg HCB/kg/day. It seems that the daily HCB intake by residents of communities surrounding Magnola will not be likely to exceed this RfD. The TDI of TCDD is 10pg/kg body wt/day. Hence, a person who weighs 50kg can tolerate a maximum of 500pg/person/day. The aforementioned TCDD intake of 20pg/person/day in the Netherlands is below the maximum tolerable daily intake. This suggests that dioxin intakes by the general population are well below the TDI.

Conclusions and Recommendations

Magnola magnesium extraction plant is not at its full operation capacity yet, and it only intends to measure HCB and dioxin levels in the air three times a year. However, this may not truly reflect the distribution of these substances in the air under all weather conditions. Moreover, because the projected air HCB levels in the vicinity of Magnola is more than double that of air HCB levels from other locations around the world, the air quality monitoring program should attempt to provide data on HCB levels in the air at shorter time intervals to allow proper assessment. In addition, the monitoring program should start immediately in order to provide a frame of reference in the future. In other words, this will allow future researchers determine the changes in air quality, particularly air HCB concentration, attributable to Magnola.
It appears that the workers at the magnesium extraction plant will have a higher level of body HCB burden. It is therefore imperative for the company to create occupational hygiene education programs so that workers can avoid excessive exposure.
It is in the general population's best interest to measure the blood HCB level before the plant reaches its full capacity. This will allow future studies to have a frame of reference, and a more accurate estimate of increase in HCB concentration attributable to Magnola will be possible. In addition to blood samples, another good indicator of HCB burden in the human body is the amount of pentachlorobenzenethiol (PTBC) in the urine samples (To-Figueras et al. 1997). Such data should also be collected now for future comparisons.
Moreover the use of oral contraceptives and alcohol consumption by residents in communities around Magnola should be examined. The reasons are that increased reported cases of porphyria in women of childbearing may be related to the use of oral contraceptives (De Mola et al. 1996), and middle-aged males who indulge in alcohol consumption are the most common porphyria patients (Baxi et al. 1983).
The potential adverse health effects due to exposure to HCB and dioxins are not limited to the five effects discussed in this section. Currently researchers are investigating the action mechanism of HCB on skin, lung and immune system (Michielsen et al. 1999), and as mentioned above the threshold level of adverse health effects by chronic HCB exposure is yet to be determined (To-Figueras et al. 2000). Therefore, this report should be updated later.