Polychlorinated Biphenyls (PCBs): Industrial Toxins in Our Environment

Table of Contents

  1. Overview
  2. Sources of Exposure
  3. Mechanism of Toxicity
  4. Health Effects
  5. PCBs in the Food Supply
  6. Body Burden
  7. Detoxification and Reduction Strategies
  8. Regulatory Framework
  9. Recent Research and Advances
  10. Related Topics
  11. References

1. Overview

Polychlorinated biphenyls (PCBs) are a class of synthetic organic chemicals consisting of a biphenyl backbone — two connected benzene rings — to which between one and ten chlorine atoms can be attached at various positions. This structural flexibility gives rise to 209 theoretically possible congeners, numbered PCB-1 through PCB-209 according to the IUPAC-based Ballschmiter and Zell numbering system. Of these 209 congeners, approximately 130 were found in commercial PCB mixtures, and around 70 have been detected in environmental and biological samples.

PCBs were first synthesized in 1881 by Schmidt and Schultz, but large-scale industrial production began in the United States in 1929 when Monsanto Company (then known as Swann Chemical Company, which Monsanto acquired in 1935) began manufacturing PCBs under the trade name Aroclor. The Aroclor numbering system encodes both the biphenyl backbone and chlorine content: for example, Aroclor 1242 contains a biphenyl base (12) with approximately 42% chlorine by weight, while Aroclor 1254 contains about 54% chlorine. Aroclor 1260, with 60% chlorine, was among the most heavily chlorinated commercial mixtures produced. Other countries produced analogous products under different trade names: Kanechlor (Japan), Clophen (Germany), Fenclor (Italy), and Sovol (USSR).

Because of their remarkable chemical stability, low flammability, high boiling points, and excellent electrical insulating properties, PCBs were embraced by industry for a wide range of applications throughout the mid-twentieth century. Major uses included dielectric fluids in electrical transformers and capacitors, hydraulic fluids, lubricating oils, plasticizers in paints and adhesives, carbonless copy paper, caulking compounds in buildings, fluorescent light ballasts, heat transfer fluids, and flame retardants in plastics. Between 1929 and 1977, an estimated 1.5 billion pounds (680,000 metric tons) of PCBs were produced in the United States alone.

Evidence of widespread environmental and health harm accumulated through the 1960s and 1970s. The 1968 Yusho disease outbreak in Japan, in which over 1,800 people were poisoned by PCB-contaminated rice oil, provided a stark demonstration of PCBs' acute and chronic toxicity. In 1976, the U.S. Congress passed the Toxic Substances Control Act (TSCA), and in 1979 the U.S. Environmental Protection Agency banned the manufacture, processing, and distribution of PCBs except in totally enclosed systems. By this time, however, an estimated 370,000 metric tons of PCBs had already been released into the global environment.

Internationally, PCBs were listed among the original twelve persistent organic pollutants (POPs) — the "dirty dozen" — under the Stockholm Convention on Persistent Organic Pollutants, which entered into force in 2004 and has been ratified by over 180 countries. The Convention calls for the elimination of PCB use in equipment by 2025 and environmentally sound management of PCB-containing waste by 2028. Despite these international commitments, PCBs continue to circulate in the global environment due to their extraordinary persistence. They resist biodegradation, bioaccumulate in fatty tissues, and biomagnify up food chains — a process in which tissue concentrations increase at each successive trophic level, sometimes by factors of 1,000-fold or more from water to top predators.

2. Sources of Exposure

Legacy Contamination in Buildings and Equipment

Despite the 1979 U.S. ban, PCBs remain present in an enormous amount of pre-1979 infrastructure. Electrical transformers and capacitors manufactured before the ban may still contain PCB-laden dielectric fluids, particularly in older industrial facilities, utilities infrastructure, and some developing countries where equipment lifespans are extended. Leaking or damaged transformers represent point sources of PCB contamination in soil and groundwater.

One of the most underappreciated sources of ongoing human exposure is PCB-containing caulking and sealants in buildings constructed or renovated between approximately 1950 and 1979. Polysulfide-based caulks used extensively in concrete construction, particularly in schools, universities, and commercial buildings, frequently contained PCBs — in some cases at concentrations exceeding 100,000 mg/kg (10% by weight). Studies of urban schools in the United States and Europe have documented elevated indoor air PCB concentrations in buildings with intact but aging PCB-containing caulk, sometimes exceeding EPA guidance values by factors of ten or more. PCBs volatilize from caulk at room temperature and sorb onto dust particles, creating both inhalation and dermal exposure routes for building occupants.

Fluorescent light ballasts manufactured before 1979 in the United States, and somewhat later in other countries, commonly contained PCB-filled capacitors. When these ballasts fail and overheat, they can release PCBs into indoor air and deposit contamination in ceiling spaces. Many older commercial and institutional buildings still contain PCB ballasts that have not been replaced.

Food Chain Contamination

For the general population without occupational exposure or residence near known contaminated sites, diet is the primary route of PCB exposure, accounting for approximately 90% of total intake. Because PCBs are lipophilic (fat-soluble), they concentrate in animal fat. The highest dietary exposures come from fatty fish from contaminated waterways, followed by other animal products including dairy, meat, and poultry.

Contaminated waterways represent the entry point of PCBs into aquatic food chains. Sediment-bound PCBs are taken up by bottom-dwelling organisms, which are consumed by small fish, which are consumed by larger predatory fish. By the time PCBs reach a large fish such as a striped bass, lake trout, or bluefish, tissue concentrations may be millions of times higher than concentrations in the surrounding water.

Farmed Atlantic salmon has been a subject of particular concern. A landmark 2004 study by Hites et al. published in Science analyzed 459 farmed and wild salmon samples from around the world and found that farmed salmon contained significantly higher concentrations of PCBs and other organochlorine contaminants than wild Pacific salmon. Mean PCB concentrations in farmed salmon ranged from approximately 27 to 80 ng/g (parts per billion, wet weight) depending on origin, compared to 0.6 to 5 ng/g in wild Pacific salmon species. The elevated contamination in farmed salmon was attributed to fish meal and fish oil in aquaculture feed, which concentrates persistent organic pollutants from the small forage fish used in feed production.

Contaminated Sites

Several sites in the United States represent severe legacy PCB contamination that continues to affect local communities and food supplies:

Indoor Air in Pre-1979 Buildings

Multiple studies have documented elevated PCB concentrations in indoor air of buildings constructed before 1979. A study of New York City schools found median indoor air PCB concentrations exceeding 100 ng/m³ in buildings with PCB-containing caulk, compared to outdoor ambient air concentrations typically below 1 ng/m³. Children in such environments may receive PCB doses from inhalation and dust ingestion that rival or exceed dietary intake. Remediation of PCB-containing caulk in occupied buildings is technically challenging and expensive, and many schools and public buildings have not been remediated.

3. Mechanism of Toxicity

Dioxin-Like vs. Non-Dioxin-Like PCBs

PCB congeners are broadly divided into two mechanistic categories based on their molecular geometry and primary mechanism of toxicity. This classification has important implications for risk assessment and regulatory standards.

Dioxin-like PCBs (DL-PCBs) include approximately 12 congeners that possess a planar molecular configuration and act primarily through the aryl hydrocarbon receptor (AhR), the same mechanism employed by the highly toxic 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Planarity is achieved when PCBs have no chlorine substitutions at the ortho positions (positions 2, 2', 6, and 6' on the biphenyl rings), allowing the two phenyl rings to adopt a coplanar conformation. The most toxicologically important dioxin-like PCB congeners include PCB-77 (3,3',4,4'-tetrachlorobiphenyl), PCB-126 (3,3',4,4',5-pentachlorobiphenyl), and PCB-169 (3,3',4,4',5,5'-hexachlorobiphenyl). PCB-126 is the most potent dioxin-like PCB congener and carries a toxic equivalency factor (TEF) of 0.1 relative to TCDD.

AhR activation by dioxin-like PCBs triggers a well-characterized signaling cascade: the PCB-AhR complex translocates to the nucleus, dimerizes with the AhR nuclear translocator (ARNT) protein, and binds to dioxin response elements (DREs) in the promoters of target genes. This upregulates expression of cytochrome P450 enzymes (particularly CYP1A1, CYP1A2, and CYP1B1), which in turn generate reactive oxygen species and metabolize hormones, drugs, and endogenous signaling molecules. Chronic AhR activation promotes inflammation, immune dysregulation, altered steroid hormone metabolism, and carcinogenesis.

Non-dioxin-like PCBs (NDL-PCBs) include the majority of PCB congeners and tend to have chlorine substitutions at ortho positions, preventing coplanar conformation and therefore have low AhR affinity. They exert toxicity through multiple other mechanisms, many of which are neurologically relevant. NDL-PCBs are often more abundant in commercial mixtures and biological samples than DL-PCBs.

The TEQ System

Because DL-PCBs and dioxins share the AhR mechanism, their combined toxicity can be expressed using the toxic equivalency (TEQ) system. Each congener is assigned a TEF relative to TCDD (TEF = 1.0). The total TEQ for a sample is calculated by multiplying the concentration of each DL-PCB congener by its TEF and summing the results. The World Health Organization (WHO) periodically updates TEF values; the current WHO-2005 TEF scheme is widely used in regulatory and risk assessment contexts. TEQ calculations allow the combined dioxin-like activity of complex mixtures to be expressed as a single number equivalent to a mass of TCDD.

Neurotoxic Mechanisms

NDL-PCBs exert neurotoxicity through several mechanisms that are distinct from AhR activation:

4. Health Effects

Cancer

The International Agency for Research on Cancer (IARC) classified PCB mixtures (polychlorinated biphenyls) as Group 1: Carcinogenic to Humans in 2016, upgrading from the previous Group 2A (probably carcinogenic) classification. This upgrade was based on sufficient evidence of carcinogenicity in humans for non-Hodgkin lymphoma and malignant melanoma, as well as mechanistic evidence supporting carcinogenicity through multiple pathways. Animal studies demonstrate carcinogenicity at multiple sites including liver, thyroid gland, pituitary gland, adrenal gland, and others.

Cohort studies of workers with occupational PCB exposure have found elevated risks for non-Hodgkin lymphoma, malignant melanoma, breast cancer, rectal cancer, and liver cancer. A landmark study of workers at two Monsanto PCB manufacturing plants (capacitor and transformer manufacturing) in Indiana found significantly elevated mortality from non-Hodgkin lymphoma and rectal cancer. Studies of Great Lakes fishing communities with high dietary PCB exposure have found associations with breast cancer, non-Hodgkin lymphoma, and liver cancer.

Neurodevelopmental Effects

Prenatal and early-life PCB exposure is among the most thoroughly documented and consequential health effects. Multiple prospective birth cohort studies across different countries and exposure contexts have found associations between maternal blood or cord blood PCB levels and impaired cognitive development in children:

The neurodevelopmental effects of PCBs are considered particularly serious because they occur at low doses during critical developmental windows, are largely irreversible, and affect IQ and behavior in ways that have lifelong consequences for individuals and societal costs for populations.

Endocrine Disruption

PCBs are well-established endocrine-disrupting chemicals (EDCs) that interfere with multiple hormonal systems:

Immune Suppression

PCBs suppress multiple aspects of immune function. Animal studies demonstrate dose-dependent reductions in thymus weight, lymphocyte counts, antibody responses, and natural killer cell activity following PCB exposure. In humans, occupational and environmental PCB exposures have been associated with altered lymphocyte subpopulations, reduced antibody responses to vaccines, and increased susceptibility to infections. The Yusho poisoning victims in Japan showed long-term immune dysfunction decades after the acute exposure event. Children with higher prenatal PCB exposure have shown impaired antibody responses to childhood vaccines in several prospective studies.

Liver Damage

The liver is a primary target organ for PCB toxicity due to its role in biotransformation. Hepatotoxicity manifests as elevated liver enzymes (ALT, AST, GGT), hepatomegaly, fatty liver, and at higher exposures, necrosis. In the Yusho and Yucheng (Taiwan, 1979) PCB poisoning incidents, many victims developed significant liver disease. Occupational studies have found elevated rates of liver disease among PCB-exposed workers. DL-PCBs induce CYP1A2 in the liver, which has been used as a biomarker of exposure.

Skin Effects and Chloracne

Chloracne is a severe and distinctive form of acne-like skin eruption that is pathognomonic of dioxin and DL-PCB exposure. It was a prominent feature of the Yusho incident, where victims developed extensive chloracne along with darkening of the skin and mucous membranes (a condition termed sho-yu coloration), nail and hair abnormalities, and ocular discharge. Chloracne lesions are comedones (blackheads and whiteheads), cysts, and pustules that preferentially affect the face, particularly the malar region and behind the ears, and can extend to the trunk and limbs in severe cases. Unlike common acne, chloracne is refractory to standard treatment and may persist for years after cessation of exposure.

Cardiovascular Effects and Diabetes Risk

Epidemiological evidence links PCB exposure to elevated risk of cardiovascular disease, including hypertension, coronary artery disease, and stroke. A meta-analysis of 19 studies found a statistically significant association between PCB exposure and cardiovascular mortality. Proposed mechanisms include PCB-induced dyslipidemia, oxidative stress, endothelial dysfunction, and inflammation.

Several large population studies have found associations between PCB body burden and elevated risk of type 2 diabetes. A meta-analysis by Codru et al. found a dose-response relationship between blood PCB levels and diabetes prevalence in the general U.S. population (NHANES data). The mechanism may involve PCB interference with insulin signaling, glucose metabolism, pancreatic beta-cell function, and adipogenesis.

5. PCBs in the Food Supply

Fish Consumption Advisories

Fish consumption advisories for PCBs are among the most widespread food safety interventions in the United States. The FDA has established an action level of 2 parts per million (ppm, wet weight) for PCBs in fish and shellfish destined for interstate commerce, above which fish must be removed from commercial sale. The EPA recommends a lower level of 0.2 ppm for subsistence fishing populations consuming fish over a lifetime. Individual states issue consumption advisories for specific waterbodies that often recommend limiting or avoiding consumption of certain species caught in particular locations.

As of 2024, virtually all major river systems in the northeastern and Great Lakes regions of the United States have at least some PCB-related fish advisories. The FDA Total Diet Study regularly monitors PCB levels in foods available in the commercial marketplace.

Farmed vs. Wild Salmon

The 2004 Hites et al. Science study provided quantitative data comparing PCB burdens in farmed and wild salmon from different global regions. Key findings included:

The study authors estimated that consumption of farmed Atlantic salmon at rates that maximize cardiovascular health benefits (approximately two meals per week) would expose consumers to PCB levels that, according to EPA cancer risk guidelines, would exceed acceptable cancer risk thresholds. The salmon aquaculture industry disputed these conclusions, and subsequent studies with improved feed PCB content suggested that farmed salmon PCB levels declined somewhat after the publication. However, independent monitoring continues to document higher PCB levels in farmed versus wild salmon, with the magnitude of difference varying by geographic origin and feed composition.

Great Lakes Fish

Great Lakes fish remain among the most PCB-contaminated food sources widely available in the United States. Lake trout (Salvelinus namaycush) and coho and Chinook salmon accumulated particularly high PCB tissue concentrations due to their position at the top of the Great Lakes food chain and their high fat content. Multiple studies in the 1980s and 1990s documented PCB concentrations in Lake Michigan lake trout and coho salmon ranging from 5 to 25+ ppm in some sampling periods — well above both the FDA action level and EPA risk-based values. PCB concentrations in Great Lakes fish have declined substantially since the 1970s due to the production ban and reduced industrial discharges, but levels in predatory species remain elevated relative to most ocean fish.

Dairy, Meat, and Poultry

Beyond fish, animal fat in dairy products, beef, pork, and poultry represents an important dietary PCB exposure route for populations with average fish consumption. PCBs accumulate in livestock primarily through contaminated feed ingredients (fish meal, animal by-product meals) and atmospheric deposition onto pastureland. While individual animal product PCB concentrations are typically much lower than those found in highly contaminated fish, high consumption volumes make these foods significant contributors to population-level PCB exposure. European monitoring data consistently detect PCBs in butter, cheese, beef fat, and chicken fat, generally in the range of 0.5 to 5 ng/g fat.

Breast Milk Levels

Human breast milk is a sensitive indicator of maternal PCB body burden and represents a potentially significant route of infant exposure. PCBs are readily transferred from maternal adipose stores into breast milk lipid, with breast milk concentrations roughly proportional to blood levels. Population monitoring studies in industrialized countries have found median breast milk PCB concentrations ranging from approximately 50 to 200 ng/g lipid, with higher values in older women (reflecting longer bioaccumulation) and women with high fish consumption. Despite the potential for PCB exposure through breast milk, health authorities universally recommend continued breastfeeding because the known benefits of breastfeeding substantially outweigh the risks from PCB exposure in the vast majority of situations.

6. Body Burden

Adipose Storage and Half-Lives

PCBs partition strongly into adipose tissue, where they may remain for years to decades. The rate of elimination from the body depends critically on the degree of chlorination: lower-chlorinated congeners (fewer than five chlorines) are metabolized more readily by hepatic cytochrome P450 enzymes and have shorter biological half-lives, measured in weeks to months. Higher-chlorinated congeners (five or more chlorines) are extremely resistant to metabolic attack and have estimated biological half-lives in human adipose tissue of 10 to 15 years or longer. PCB-180 (2,2',3,4,4',5,5'-heptachlorobiphenyl), one of the most abundant congeners in human adipose tissue due to its environmental persistence and resistance to metabolism, has an estimated half-life in the human body exceeding 10 years. This means that even with complete cessation of exposure, body burdens of the most persistent congeners decline only very slowly.

Biomonitoring Data — NHANES

The U.S. National Health and Nutrition Examination Survey (NHANES) has measured serum PCB levels in representative samples of the U.S. civilian non-institutionalized population since the 1970s. Key findings from NHANES data include:

Generational Transfer

One of the most concerning aspects of PCB body burden is its potential for generational transfer. PCBs cross the placental barrier and accumulate in fetal tissues; cord blood PCB concentrations are typically 60–80% of maternal blood concentrations. Additionally, breast milk transfer during lactation can further add to the infant's body burden. Studies of mothers who themselves had elevated prenatal PCB exposure (as children of women who consumed contaminated Great Lakes fish) found measurable PCB levels in their cord blood, demonstrating transgenerational carryover of contamination. This means that PCB exposures that occurred decades before the current generation was born continue to affect fetal development today.

7. Detoxification and Reduction Strategies

Dietary Approaches

Because PCBs are stored in fat and eliminated primarily via biliary excretion into the intestine, strategies that either reduce adipose mobilization into blood or enhance fecal excretion of PCBs have theoretical and some empirical support:

Fish Selection

For individuals who consume fish regularly, selection of species and source can significantly affect PCB exposure. Generally lower-PCB choices include:

Fish with higher PCB burdens that may warrant limited consumption include lake trout, bluefish, striped bass, and farmed Atlantic salmon from high-PCB regions. Checking state fish consumption advisories for locally caught fish is always advisable.

Olestra Research

Olestra (sucrose polyester), a fat substitute approved by the FDA for use in snack foods, is not absorbed in the intestine and has been investigated as a potential vehicle for promoting the fecal excretion of lipophilic contaminants including PCBs. A 2002 clinical study by Redgrave et al. found that daily olestra consumption significantly increased fecal excretion of dioxins and PCBs in volunteers. The effect was attributed to PCBs partitioning from body fat into the unabsorbed olestra in the intestinal lumen during enterohepatic cycling. While this research is intriguing, olestra causes gastrointestinal side effects (particularly at high doses) and is not approved as a therapeutic agent for PCB detoxification.

Exercise Caution

Exercise-induced fat mobilization releases PCBs stored in adipose tissue into the bloodstream, which transiently elevates serum PCB concentrations during and after intense exercise. While chronic regular exercise reduces total body fat and may ultimately lower total PCB body burden, the transient mobilization during heavy exercise has prompted discussion about whether rapid, extreme weight loss (e.g., crash dieting or extreme exercise regimens) could transiently increase circulating PCB levels and associated toxicity risks. Moderate, sustained exercise and gradual weight loss are preferred approaches that maximize health benefits while minimizing potential for PCB mobilization.

8. Regulatory Framework

Toxic Substances Control Act (TSCA), 1976

The U.S. Toxic Substances Control Act, enacted in 1976 and significantly amended in 2016 by the Frank R. Lautenberg Chemical Safety for the 21st Century Act, gave the EPA authority to regulate chemical substances. TSCA Section 6(e) specifically addressed PCBs, authorizing the EPA to ban PCB manufacture, processing, and commercial distribution. In 1979, the EPA issued regulations under TSCA Section 6(e) that prohibited PCB manufacture in the U.S. and restricted use to totally enclosed systems. The regulations also established disposal requirements for PCB-containing equipment and waste. The EPA subsequently promulgated cleanup standards for PCB-contaminated sites, spill cleanup policies, and remediation criteria under TSCA.

Stockholm Convention

The Stockholm Convention on Persistent Organic Pollutants, adopted in 2001 and in force since 2004, is the principal international instrument for controlling POPs including PCBs. Under the Convention:

As of 2024, 185 parties have ratified the Stockholm Convention. The United States signed but has not ratified the Convention, though U.S. domestic regulations under TSCA are broadly consistent with Convention obligations.

EPA Superfund Sites

PCB contamination is a feature of numerous sites on the EPA's National Priorities List (NPL) — the Superfund list of the nation's most contaminated sites requiring long-term cleanup action. Major PCB Superfund sites include the Hudson River (New York), New Bedford Harbor (Massachusetts), Sangamo Electric/Crab Orchard National Wildlife Refuge (Illinois), the Housatonic River (Massachusetts/Connecticut — contaminated by General Electric's Pittsfield facility), and the Anniston PCB site (Alabama). Total Superfund cleanup costs at PCB-contaminated sites have reached into the billions of dollars.

FDA Action Levels and EPA Risk-Based Values

The FDA action level of 2 ppm for PCBs in fish applies to commercial interstate commerce. This level was established in 1984 and is based primarily on analytical capabilities at the time and economic considerations, not solely on health-protective risk assessment. The EPA's more recent risk-based fish tissue concentration for PCBs, based on cancer risk calculations using a 2 × 10⁻⁵ lifetime cancer risk for a person consuming fish daily, is substantially lower at approximately 0.2 ppm — an order of magnitude below the FDA action level. This discrepancy means that fish legally sold in interstate commerce may still pose cancer risks exceeding EPA's acceptable thresholds if consumed at high rates over a lifetime.

9. Recent Research and Advances

Research on PCBs continues to evolve, with several active areas of investigation:

Neurological disease associations: Recent epidemiological and experimental research has strengthened the case for PCB involvement in Parkinson's disease. A 2017 study by Hatcher-Martin et al. found that Georgians living near a former PCB manufacturing facility had elevated Parkinson's disease prevalence. Mechanistic research has identified disruption of dopaminergic pathways, mitochondrial dysfunction, and neuroinflammation — all features of Parkinson's disease — as consequences of PCB exposure in animal models. The hypothesis that PCBs may trigger or accelerate alpha-synuclein aggregation (the pathological hallmark of Parkinson's disease) is under active investigation.

Epigenetic effects: Growing evidence indicates that PCB exposure can alter DNA methylation patterns, histone modifications, and microRNA expression. These epigenetic changes may mediate some of PCBs' developmental and carcinogenic effects and could potentially be transmitted to subsequent generations. A 2020 study found altered DNA methylation at immune-related genes in children with higher prenatal PCB exposure, suggesting epigenetic mechanisms may underlie PCB-associated immune dysregulation.

Mixture effects and low-dose concerns: Traditional toxicological risk assessment evaluates individual chemicals in isolation, but humans are exposed to complex mixtures of PCB congeners simultaneously with dioxins, furans, other organochlorines, and diverse environmental contaminants. Research on mixture effects has generally found that PCBs interact additively or sometimes synergistically with other AhR ligands and neurotoxicants, suggesting that risk assessments based on individual compounds may underestimate actual risk. The concept of the "exposome" — the totality of environmental exposures throughout life — has become an important framework for understanding PCB effects in the context of real-world multi-chemical exposure.

Remediation technology advances: Novel approaches to PCB-contaminated sediment remediation are under development and evaluation. These include in situ activated carbon amendment (adding powdered or granular activated carbon to contaminated sediment to bind PCBs and reduce their bioavailability), bioremediation using PCB-degrading bacteria such as Burkholderia xenovorans LB400 and Rhodococcus species capable of oxidizing lower-chlorinated congeners after reductive dechlorination by anaerobic bacteria, and enhanced natural recovery monitoring approaches. The combination of anaerobic reductive dechlorination (which removes chlorines from higher-chlorinated congeners, making them more susceptible to aerobic oxidation) followed by aerobic biphenyl-oxidizing bacteria represents a potentially complete bioremediation pathway that is the subject of ongoing field trials.

Building PCB remediation: Improved methods for identifying, quantifying, and remediating PCB-containing caulk in occupied buildings have been developed. Research at Harvard and Boston University has characterized the dynamics of PCB volatilization from caulk, the role of HVAC systems in distributing PCBs through buildings, and the effectiveness of different remediation approaches including caulk removal, caulk encapsulation, and enhanced ventilation. Cost-effectiveness analyses of building PCB remediation in schools have shown that remediation can be cost-effective in reducing lifetime cancer risk when PCB air concentrations are sufficiently elevated.

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