Public Information and Records Integrity Branch (PIRIB)

Information Resources and Services Division (7502C)

Office of Pesticide Programs (OPP)

Environmental Protection Agency

1200 Pennsylvania Avenue, NW

Washington, DC  20640

Docket Control Number OPP-34239 – Lindane Preliminary Risk Assessment

Comments Submitted on Behalf of:

Natural Resources Defense Council

Commonweal

Institute for Agriculture and Trade Policy

Northwest Coalition for Alternatives to Pesticides

Physicians for Social Responsibility-Los Angeles

Physicians for Social Responsibility-San Francisco Bay Area

Washington Toxics Coalition

By Gina M. Solomon, M.D., M.P.H.

Senior Scientist

October 29, 2001

The Natural Resources Defense Council (NRDC), Commonweal, the Institute for Agriculture and Trade Policy (IATP), the Northwest Coalition for Alternatives to Pesticides (NCAP), Physicians for Social Responsibility Los Angeles and San Francisco Bay Area Chapters (PSR), and the Washington Toxics Coalition (WTC) appreciate the opportunity to comment on the risk assessment and RED for lindane. We are submitting these comments on behalf of our over 500,000 members nationwide, and particularly our members in the Northwestern United States. Many of our members are pregnant or have children who may be disproportionately exposed and susceptible to the health effects of a neurotoxic and endocrine disrupting chemical such as lindane. We receive calls from our members, and members of the general public, with questions related to exposure to lindane used for treatment of head lice or scabies. Our work has focused for decades on risks to infants and children from exposure to toxic chemicals, pesticides, and endocrine disruptors. Our groups are therefore directly affected by EPA’s RED and risk assessment for lindane. None of our organizations have any financial interest in the manufacture or use of lindane or lindane-containing products.

Overview of Lindane Toxicity

Lindane, also known as gamma-hexachlorocyclohexane (g-HCH), is a persistent organic pollutant in the organochlorine pesticide class. Most organochlorine pesticides have been banned due to their toxicity, environmental persistence, and tendency to bioaccumulate. Lindane shares all three of these highly undesirable characteristics with its sister organochlorine pesticides, yet to date it has somehow evaded appropriate regulation and elimination.

This chemical is highly persistent in a soil, with a half-life of more than a year, and has been found to contaminate the Great Lakes, and in groundwater in New Jersey, California, Mississippi, and South Carolina. Lindane residues have been reported in a variety of fatty foods such as hamburger, frankfurters, fish, bologna, peanuts, butter, cookies, and candy bars.[1] Residues in fatty foods are due to the fact that this chemical tends to accumulate and concentrate in fat.

Lindane is a known neurotoxicant in humans, and it has been reported to cause seizures and other adverse effects in children treated for head lice. Other effects reported in humans following exposure include tremors, memory impairment, irritability, and aggression.[2]  To our knowledge, long-term studies looking at potential long-term impacts on children exposed to lindane have not been well investigated. In animal studies, lindane is known to suppress levels of dopamine and norepinephrine, critical neurotransmitters.[3]  At lower doses, lindane causes abnormal behavior patterns, abnormal brain wave patterns on electroencephalogram (EEG), hyper- or hypoactivity, interference with learning, temperature dysregulation, and anxiety.[4]

Lindane is a known endocrine disruptor in animals, and is associated with a range of serious effects on reproduction and development.  These effects include testicular damage, reduced sperm production, disrupted estrus (menstrual) cycles, delayed puberty in females, ovarian and uterine atrophy, and infertility.[5] Adult male rats treated with lindane develop atrophy of their sex accessory organs, including the epididymis, seminal vesicles, and vas deferens, consistent with treatment with an anti-androgen.[6] The same investigators also identified decreases in testicular weight and degeneration of the Leydig cells, resulting in diminished testosterone levels in adult male rats dosed with lindane.[7]

Lindane is a weak estrogen, a more potent anti-estrogen and anti-androgen, and may also interfere with thyroid and adrenal gland function. Ewes fed lindane have significantly decreased thyroid hormone (thyroxine) and pituitary hormone (LH) concentrations and significantly increased insulin and estrogen levels.[8] In adult female mice, administration of lindane results in atrophy of the adrenal glands and abnormalities of the gland structure. The mice also have increased cholesterol levels and decreases in ascorbic acid (Vitamin C) content of the glands.[9]

Low, environmentally relevant, doses of lindane inhibit the binding and production of androgens in the prostate, even at the tiniest dose tested. The inhibition does not appear to occur via direct binding to the androgen receptor. These investigators reported a synergistic interaction between malathion and lindane resulting in inhibition of  testosterone metabolism in the rat prostate.[10]

One European study of women with reproductive problems identified elevated levels of lindane in the blood of women with infertility and menstrual dysfunction. Exposure to lindane was from off-gassing of treated wood used in home construction. Removal of the exposure resulted in normalization of menstruation.  Although this study does not conclusively prove a link between lindane and reproductive abnormalities in humans, the results are consistent with animal studies in numerous species.[11]

Major Concerns with EPA’s Lindane Risk Assessment

While NRDC, Commonweal, IATP, NCAP, PSR, AND WTC are pleased that most pesticidal uses of lindane have been eliminated in recent years, we are very concerned by serious omissions in the EPA draft risk assessment that will tend to underestimate human health risks and environmental risks from the remaining uses of this very toxic chemical. In particular, we were appalled by the narrow scope of the risk assessment, and by repeated violations of EPA’s legal obligation to consider all exposure pathways. It is illegal and scientifically incorrect to ignore known exposures to lindane from pharmaceutical uses, pet care, breast milk contamination, bioaccumulation in fish, and from past uses of this persistent chemical.

In addition, it is dangerous and irresponsible to reduce the 10x factor designed to protect children for a pesticide such as lindane that poses a major risk to children’s health and for which the toxicology database is acknowledged to be incomplete.  Lindane is known to be transformed in the environment and in living organisms into the even more dangerous isomer b-HCH, yet although EPA acknowledges that this does occur, the risks from this isomer was not included in the assessment. Lindane is a serious threat to drinking water, yet the EPA risk assessment is misleading in its underestimate of the acknowledged threat. Finally, EPA’s risk assessment reveals disturbingly high risks to workers handling lindane; the “true” risks are likely far higher because EPA fails in its assessment to combine inhalation and dermal exposures when evaluating risks to workers.

Failure to Include Topical Use of Lindane for Lice and Scabies

The Agency is well aware that the greatest exposure of children to lindane comes from direct application of the pesticide to their scalp or body for treatment of head lice or scabies. Numerous childhood poisonings have been reported to FDA and in the medical literature from lindane applied in this manner. Reported acute health effects include nausea, vomiting, CNS stimulation, and seizures.[12] Although EPA mentions this important exposure pathway in the risk assessment, it is completely omitted from all quantitative calculations in the document. Instead the document adopts the fiction that the only child exposures are through use as a seed treatment. This approach is in clear violation of the FQPA.

EPA is required by law to consider “available information concerning the aggregate exposure levels of consumers (and major identifiable subgroups of consumers) to the pesticide chemical residue and to other related substances, including dietary exposure under the tolerance and all other tolerances in effect for the pesticide chemical residue, and exposure from other non-occupational sources.” [emphasis added] (FFDCA as amended by the FQPA §408(b)(2)(D)(vi)) The law does not say that EPA only need include exposure pathways that are within its regulatory jurisdiction. Therefore it is clear that pharmaceutical uses of lindane must be included in the risk assessment. EPA cannot legally proceed to issue any final rules or tolerances based on a risk assessment that fails to even consider the main exposure pathway for children to lindane.

NRDC scientists are of the opinion that including all exposure pathways for lindane will reveal risks to children that are highly significant and potentially hazardous.  This opinion is supported by a calculation performed by the Sanitation Districts of Los Angeles County, showing that: (a) typical lindane application rates for lice and scabies are one ounce of a one percent lindane formulation for children under six and one to two ounces for older children and adults; (b) a topical application of one ounce of lotion (28 ml) amounts to an applied dose of 0.28 g of lindane; (c) using a best case 10% absorption factor, a ten pound infant would absorb 6 mg/kg, which is equal to the NOAEL of lindane.  If this is the case, EPA must transmit these results immediately to the FDA and must suspend all uses of lindane that are within its jurisdiction.

On November 5, 1979 (44 Federal Register, 63749), EPA exempted lindane lice and scabies products from the requirements of the FIFRA, stating: “EPA and FDA concluded that the dual review of pesticide/new drug products offered solely for human use represents an expensive duplication of time and resources for both the Agencies and the sponsors of these products without any significant increase in benefits to public health and/or the environment.  It is further concluded that regulations of these products solely by FDA under the FFDCA would adequately serve the intent of FIFRA.” 

Since 1979, the situation has changed, most notably with passage of the Food Quality Protection Act of 1996 (FQPA) requiring EPA to review all pesticide registrations to make sure that they are safe. No similar provisions exist under the FFDCA.  We are asking EPA to reassert its control over lice and scabies treatments under the FIFRA. Or, at minimum, EPA must consider the human health and environmental impacts of these treatments in its current risk assessments. As lindane lice and scabies products dominate the human health and environmental risks of lindane, the risk assessments are meaningless without them.  Under the FIFRA, EPA has a statutory responsibility to ensure that pesticides are safe and effective for their intended uses and to prevent unreasonable adverse effects to man, other animals, and the environment from their usage (7 U.S.C. §136(bb), §136a(a), §136a(d)(2); §136d(b)).  By ignoring the risks posed by lindane lice and scabies treatments, EPA is not fulfilling its statutory responsibility. 

EPA mentions in one place in the RED that the registrant plans to maintain the registration for lindane use in pet care. If this is true, then EPA needs to include this exposure pathway in the risk assessment. The Agency is well-aware of the fact that chemicals applied to the skin and fur of household pets will get on the skin of members of the household, including children who may pet, hug, or sleep with, the animals.[13] We understand that at least one manufacturer of veterinary lindane products (Happy Jack) has EPA approval to continue manufacturing their products through 12-31-01. This exposure pathway must be discussed, and EPA must make sure that veterinary uses of lindane are completely eliminated.

Failure to Include Breast Milk Exposures

NRDC, Commonweal, IATP, NCAP, PSR, AND WTC are pleased that EPA acknowledged arctic populations as a group at special risk from lindane. It is quite true that this persistent organic pollutant tends to travel to polar regions as a result of global distillation.  Lindane can be present as a vapor or can attach to small airborne particles of soil and dust. Lindane can remain in the air for up to 17 weeks, and can travel long distances. Airborne particles with attached HCH may be removed from the air by rain.[14]  Lindane has been detected in areas where it was never applied, and is known to bioaccumulate in the fish and marine mammals that make up the diet of arctic indigenous groups.

Technical grade hexachlorocyclohexane and its isomers have been found in breast milk throughout the world.[15] [16] [17]  HCH breaks down more slowly in temperate climate zones than in the tropics.[18]  Thus, levels of HCH in the environment, and in breast milk, are likely to be relatively higher in cool climates. The concentration of HCH in breast milk is also strongly related to diet. A German study found that women who followed a low-fat diet had lower beta-HCH levels in their breast milk than women whose diet included large quantities of meat.[19] A study of women whose diets consisted primarily of fish, found particularly high levels of HCH isomers in their breast milk.[20] Levels of lindane in breast milk in Germany remained over 5 ng/g lipid in the most recent data reported.[21]

Although the EPA risk assessment did acknowledge that lindane has been detected in breast milk, the document failed to include an exposure assessment for nursing infants in the risk assessment of the arctic population, or for the U.S. population. It is bizarre that the EPA document could admit that, “the milk:plasma concentration ratio for lindane indicates a much more efficient excretion of the compound in milk…The presence of lindane in mammalian milk exposes nursing offspring during critical periods of post-natal development (Dalsenter et al. 1997).” (p. 12 of Lindane RED Chapter: Environmental Fate and Ecological Risk Assessment) Yet at the same time, EPA fails to include a nursing infant scenario in the risk assessment. This omission is particularly egregious because lindane is known to bioaccumulate to higher levels in breast milk, and because the nursing infant is at higher risk from the neurotoxic and endocrine disrupting effects of this chemical. Failure to include the breast milk exposure pathway is another violation of §408(b)(2)(D)(vi) of the FFDCA as cited above.

Failure to Include Exposure from Fish Consumption

The EPA RED indicates that bioconcentration studies have been carried out with regard to several fish species. For example, in the case of the bluegill sunfish, bioconcentration factors are reported to be 780 for fillet, 2500 for viscera, and 1400 for whole fish tissues (p. 5 of Lindane RED Chapter: Environmental Fate and Ecological Risk Assessment). Inexplicably, however, the human health risk assessment completely ignores risks to fish eaters from bioconcentrated residues of lindane and other HCH isomers in fish. There is no question that such exposures can and do occur. Furthermore, exposures from fish consumption would not be limited to arctic populations, but would also include subsistence fishers in the United States. This oversight must be corrected in the final version.

Furthermore the risk assessment for arctic populations is flawed. The exposure estimate relies on a study of food consumption patterns among tribes in the Pacific Northwest, whose diet consists of foods quite different from the Alaskan tribes, and is generally much lower on the food chain.[22] Failure to properly include the dietary patterns of indigenous arctic populations in the exposure assessment is virtually guaranteed to substantially underestimate the exposure to these vulnerable groups.

Failure to Include Past Uses of a Persistent Chemical

In the case of pesticides that break down rapidly in the environment, EPA has the luxury of considering only exposures from the current proposed uses of that chemical. Persistent organic pollutants pose a completely different problem. Although the only proposed uses before EPA at present may involve seed treatment, it is an acknowledged fact that our environment and tissues are laced with lindane and other HCH isomers from widespread historical use of this chemical. These exposures cannot be ignored. Again, we wish to remind the EPA Administrator that the Agency is required by law to consider “available information concerning the aggregate exposure levels of consumers (and major identifiable subgroups of consumers) to the pesticide chemical residue and to other related substances, including dietary exposure under the tolerance and all other tolerances in effect for the pesticide chemical residue, and exposure from other non-occupational sources.” [emphasis added] (FFDCA as amended by the FQPA §408(b)2(D)(vi)) Historical residues that linger in our environment would be covered by this section of the law and would need to be included in the aggregate exposure assessment.

EPA Should Retain the 10x Margin of Safety to Protect Children from Lindane

EPA’s stated rationale for reducing the 10x FQPA margin of safety to 3x is deeply flawed. EPA gives six reasons for reducing the FQPA safety factor. Each of these reasons is either incorrect or irrelevant to the question before the Agency. They are discussed and refuted below:

1)      “The toxicology data base is complete”

EPA repeatedly mentions that lindane has shown endocrine disrupting effects in numerous studies submitted to EPA and in the open literature. Rather than regulating lindane as an endocrine disruptor, however, EPA states the intention to require future studies on the endocrine disrupting effects of lindane through the Endocrine Disruptor Screening and Testing Program. (see eg. Undated Memorandum from ERB IV RED Team for Lindane to B. Shackelford, Branch Chief, Special Review and Reregistration Division, regarding EFED RED Chapter for lindane, p. 3). This statement of intention amounts to an acknowledgement that there are significant data gaps in the toxicology database for lindane. If there were no data gaps, there would be no need for endocrine disruptor testing.

2)      “Available data provide no indication of increased susceptibility in rats from in utero exposure to lindane in the prenatal developmental study.”

This statement is misleading and manipulative. EPA uses three rat studies to assess fetal risk: a prenatal developmental study, a reproductive toxicity study, and a developmental neurotoxicity study. While it is true that there was no clear evidence of increased susceptibility in the first study, the other two both clearly show qualitative, and in one case, quantitative increased susceptibility in the fetus. If EPA is purporting to use a weight-of-evidence approach to assessing the scientific literature, the evidence clearly supports the disproportionate susceptibility of the fetus to the toxic effects of lindane. Furthermore, biologic plausibility also supports fetal susceptibility due to the various neurotoxic and endocrine disrupting modes of action of this chemical in the fetus and neonate. Reducing the FQPA safety factor based on one study flies in the face of the weight of scientific evidence and the mode of action of this pesticide.

3)      “The offspring effects seen in the developmental neurotoxicity study were the same as those seen in the two-generation reproduction study.”

Even if it were true, this statement would be irrelevant to the question before the Agency. The more important issue is that both of these studies clearly showed disproportionate vulnerability in the fetus. In addition, this statement is incorrect. The developmental neurotoxicity study showed increased motor activity and decreased motor activity habituation as compared to controls. These endpoints are important because they are indicative of the same type of CNS stimulation seen in human children who have been exposed to lindane. Although full-blown seizures were not observed in this particular study, these effects are along the continuum of CNS kindling and behavioral alterations that have been observed in humans. These effects were seen in the offspring in the absence of maternal toxicity. It should go without saying that CNS hyperexcitability in the offspring at doses non-toxic to the mother is indicative of a serious and very disturbing risk to the fetus, infant, and child.

4)      “Adequate actual data, surrogate data, and/or modeling outputs are available to satisfactorily assess food exposure and to provide a screening level drinking water exposure assessment.”

This rationale is rather pathetic in light of the examples presented in our comments showing that the Agency completely omits numerous exposure pathways from the risk assessment. The adequacy of the exposure data should be reconsidered after the agency evaluates and includes the data on exposure to pharmaceutical lindane, pet products, lindane in breast milk, lindane in fish, and historical residues of lindane.

5)      “Although the developmental toxicity study in rabbits was classified unacceptable, the HIARC concluded that a new study is not required.”

This rationale is also irrelevant to the decision about the 10x FQPA factor. Whether or not a new rabbit study is needed, there are obvious data gaps due to incomplete information about endocrine disrupting effects.

6)      “There are currently no residential uses.”

This is the strangest of the six reasons for abandoning the FQPA margin of safety. Most members of the public would consider direct application of lindane to a child’s skin (or to the skin of a household pet) to be a residential use. Failure to acknowledge this use of lindane has a Byzantine strangeness that baffles logic. Clearly there are residential uses. EPA must include them and must use the full 10x FQPA margin of safety because of these household uses and because none of the six justifications for abandoning the 10x holds up to logic or scientific scrutiny.

EPA Fails to Include Exposure to b-HCH

Lindane is known to be transformed in the environment and in living organisms into the even more dangerous isomer b-HCH, yet although EPA acknowledges that this does occur, the risks from this isomer was not included in the assessment.  The beta-isomer of HCH is the most persistent and bioaccumulative form. The alpha- and gamma-isomers of HCH are converted into the beta-isomer in living organisms. As a result of this conversion, as much as 90 percent of HCH detected in human tissues and breast milk is the b form of HCH.[23]  EPA must include a formal risk assessment for b-HCH exposures as a result of lindane use.

Lindane is a Serious Threat to Drinking Water

Lindane has been detected in groundwater and surface water throughout the United States. The EPA risk assessment overview states (p. 6-7): “In the USGS NAWQA study, lindane was detected in 2.58% of surface water samples (0.67% at levels greater than 0.05 ppb, maximum concentration reported was 0.13 ppb)… Although these long-term monitoring programs have detected lindane in various water bodies, the Agency determined that these data are not suitable for risk assessment, because there is no correlation of monitoring with actual lindane use.  Therefore, these data are presented here solely for informational purposes.”  2.58% of surface water samples represents one in thirty-eight samples, a significant degree of contamination for the nation’s surface water bodies. These levels must be coming from pesticidal use of lindane, including use for scabies treatment, seed treatment, and historic pesticide usage. All of these uses are relevant to a combined assessment of exposure from water, and therefore must be included in the EPA risk assessment. We disagree that these data “are not suitable for risk assessment”.  Under the Safe Drinking Water Act, the federal target for lindane levels in water bodies that are potential drinking water sources is 19 parts per trillion - well below the 11 parts per billion found in some groundwater samples as reported in the EPA STORET data base. [24]

In September 2000, the State of California banned lindane-based products used to treat lice and scabies because they wash down the drain and contaminate water supplies. Research in the Los Angeles basin in 1999 showed that lindane enters sewage systems, contaminates effluent, and enters downstream waterways.[25] The Sanitation Districts of Los Angeles County have campaigned to eliminate most lindane use because it is such a serious threat to water. According to their assessment, a single lice or scabies treatment contains enough lindane to pollute six million gallons of water to the 19 ppt standard.  Therefore, a single treatment could cause a discharge violation at a small POTW. Although it is possible that use of lindane as a seed treatment, in and of itself may not seriously threaten water supplies, EPA is obligated to consider all uses of lindane, including pharmaceutical uses, when it considers the levels of this chemical that are likely to make their way into our water.

Worker Risks are High and Underestimated

EPA’s failure to combine risks to workers from dermal exposures and inhalation exposures to lindane defies logic. NRDC, Commonweal, NCAP, PSR, and WTC understand that EPA chose to use different NOAELs with different endpoints in the dermal and the inhalation worker risk assessments. Yet it makes no sense not to combine them. It is patently obvious that an individual exposed to lindane via both skin and lungs is getting an additive dose of that chemical. It is also obvious that in worker populations such combined exposures are highly likely, and even inevitable. Persisting in the policy of considering each of these exposures separately guarantees that EPA will seriously underestimate real-world exposures to human beings that are handling this chemical on the job. That knowledge is particularly sobering in light of the fact that this ‘low-ball’ risk assessment found serious worker risks from handling lindane. NRDC is deeply concerned that workers (including pregnant and lactating women) may be exposed to dangerous levels of this chemical. EPA should combine the dermal and inhalation risk assessments and then seriously evaluate whether there are any mitigation measures that may reasonably be expected to provide adequate protection to workers. If there are no measures that will be likely to adequately protect workers, this chemical should not be registered for use on seed. The Ministry of Agriculture, Fisheries and Food in the United Kingdom ordered that all uses of lindane for seed treatment be stopped in 1999 after determining that "the level of exposure of those treating seeds with lindane is considered to be above acceptable levels."[26]

In summary, NRDC strongly advises EPA to correct the major flaws in this draft lindane risk assessment and RED. Failure to include the major exposure pathways to lindane is an affront to the scientific database on this chemical and is in contravention of the plain language of the Federal Food, Drug and Cosmetic Act as amended by the Food Quality Protection Act of 1996. On reviewing the literature on lindane’s persistence, bioaccumulation in the environment and in human tissues, and toxicity, we do not believe that this chemical can safely be registered for use in the United States. We are particularly concerned about the disproportionate risks to certain subpopulations, including fetuses, breastfeeding infants, subsistence fishing communities, and workers. We will closely monitor future EPA regulatory activities involving lindane.

[1] Food and Drug Administration. Total Diet Study: Summary of Residues Found Ordered by Pesticide Market Baskets 91-3 – 97-1, June 1999.

[2] Evangelista de Duffard AM, Duffard R.  Behavioral toxicology, risk assessment, and chlorinated hydrocarbons. Environ Health Perspect 104(suppl 2): 353-360, 1996.

[3] Ortiz Martinez A, Martinez-Conde E.  The neurotoxic effects of lindane at acute and subchronic dosages. Ecotox Environ Safety 30(2): 101-105, 1995.

[4] Llorens J, Sunol C, Tusell JM, Rodriguez-Farre E. Evidence for acute tolerance to the behavioral effects of lindane: Concomitant changes in regional monoamine status. Neuro Tox 12: 697-706, 1991.

[5] Cooper RL, Chadwick RW, Rehnberg GL, Goldman JM, Booth KC, Hein JF, McElroy WK. Effect of lindane on hormonal control of reproductive function in the female rat. Tox Appl Pharm 99:384-394, 1989.

[6] Chowdhury AR, Bhatt HV, Gautam AK, Gandhi DN. Lindane induced changes in epididymis, vas deferens and seminal vesicle in rats: Histological and pharmacological study. Ind J Physiol Allied Sci 47(4): 176-183, 1993.

[7] Chowdhury AR, Gautam AK. Steroidogenic impairment after lindane treatment in male rats. Journal of UOEH 16(2): 145-152, 1994.

[8] Rawlings NC, Cook SJ, Waldbillig D. Effects of the pesticides carbofuran, chlorpyrifos, dimethoate, lindane, triallate, trifluralin, 2,4-D, and pentachlorophenol on the metabolic endocrine and reproductive endocrine system in ewes. J Toxicol Environ Health 54(1): 21-36, 1998.

[9] Lahiri P, Sircar S. Suppression of adrenocortical function in female mice by lindane (gamma-HCH). Toxicology 66(1): 75-80, 1991.

[10] Danzo BJ. Environmental xenobiotics may disrupt normal endocrine function by interfering with the binding of physiological ligands to steroid receptors and binding proteins. Environ Hlth Persp 105(3): 294-301, 1997; Simic B, Bogojevic D, Trikic S, Kniewald J. Testosterone metabolism and formation of cytosol 5-alpha-dihydrotestosterone-receptor complex in the rat prostate in vitro: Effects of lindane and malathion. Toxicol in Vitro 6(3): 267-271, 1992.

[11] Gerhard I, Derner M, Runnebaum B. Prolonged exposure to wood preservatives induces endocrine and immunologic disorders in women. Am J Obst Gynecol 165(2): 487-488, 1991.

[12] Evangelista de Duffard AM, Duffard R.  Behavioral toxicology, risk assessment, and chlorinated hydrocarbons. Environ Health Perspect 104(suppl 2): 353-360, 1996.

[13] NRDC. Poisons on Pets: Health Hazards from Flea and Tick Products, New York, http://www.nrdc.org/health/effects/pets/execsum.asp

[14] ATSDR, ToxFAQs for Hexachlorocyclohexane, . 1995, ATSDR.

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

[16] Yakushiji, T., et al. Levels of polychlorinated biphenyls (PCBs) and organochlorine pesticides in human milk and blood collected in Osaka Prefecture from 1972 to 1977. Int Arch Occup Environ Health 1979; 43: p. 1-15.

[17] 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.

[18] Nair, A., et al. DDT and HCH load in mothers and their infants in Delhi, India. Bull Environ Contam Toxicol 1996; 56: p. 58-64.

[19] 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.

[20] 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.

[21] Furst, P., C. Furst, and K. Wilmers. Human milk as a bioindicator for body burden of PCDDs, PCDFs, organochlorine pesticides, and PCBs. Environ Health Perspect 1994; 102: p. 187-93.

[22] S. Harris and B. Harper. A Native American Exposure Scenario. 1997. Risk Analysis, Vol. 17. No. 6. pp 789-795.

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

[24] County Sanitation Districts of Los Angeles County-2, 2000. Memorandum: Supplemental Information on Lindane, March 27.

[25] Weinhold B. Last Call for Lindane. Environmental Health Perspectives 2001; 109(6): p. A254.

[26] Ministry of Agriculture, Fisheries and Food, 1999. News Release: Review of the Pesticide Lindane (206/99) June 18.