dioxins - 107.170.216.125107.170.216.125/ehib/ · common plastic) and textile dyes. dioxins in dyes...

DioxinsTechnicalInformation forCalifornia HealthOfficials

May 2003

California Department of Health ServicesEnvironmental Health Investigations Branch

3Cover Photo: Air Emissions from refineries have recently been tested for dioxins. Photo courtesy of the Society for Environmental Education

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SummaryDioxin and dioxin-like chemicals have the potential to cause harm to public health. Dioxins are contami-nants of chlorinated chemicals and incineration pro-cesses that are structurally similar, share a common biochemical mechanism, and have similar toxic effects. They are widespread and long-lasting in the environment, accumulate in the food chain, and are biologically persistent in humans. While there are still controversies about human health effects at low doses, animal and occupational studies provide evidence suggesting adverse health effects at cur-rent population exposures. Studies have established dioxin as a human carcinogen. Other studies sug-gest a possible role in a range of health problems including immune dysfunction, and endocrine and neurological effects. There is increasing scientific attention on the hazard to children. These studies imply that children may be especially vulnerable.

Most human exposure is from the fat in animal prod-ucts and fish. The World Health Organization (WHO) has estimated that dietary intake for industrialized populations is equal to, or above, their calculated Tolerable Daily Intake (TDI). The TDI is a reference level that is recognized as “safe” but incorporates only a ten-fold uncertainty factor below exposures that have been associated with adverse health out-comes. Some populations that subsist on fish from contaminated areas or that eat chicken eggs raised on contaminated soil may be at higher risk. While there is some national data available, little informa-tion is available for accurately assessing potential exposures among California residents.

In California, known sources of dioxins include industrial facilities (e.g., medical waste incinerators, sanitary services, chemical manufacturing, and refineries) and “area” sources (e.g., backyard trash

burning where plastic materials are burned, resi-dential telephone poles, land application of sewage sludge, vehicle exhaust, and chlorinated pesticides, e.g., 2,4-D). Limited air monitoring in California sug-gests similar levels to those found nationally. While direct exposures of residents to these sources are likely to be low, dioxins in the air are deposited in soil and water where they may be taken up and accumulated in the food chain.

Because of the persistence of dioxin and similar chemicals, reducing current and future exposures of the population is essential to reducing human tissue levels. Measures to reduce dioxin exposure include:

• Identifying sources and regulating stationary and mobile sources to reduce dioxin dissemination into the environment

• Educating the public to voluntarily reduce sources (such as reduction of backyard incineration and hos-pital reduction of PVC plastics in the waste stream)

• Assessing exposure pathways and concentrations of dioxins in commercial and local food sources

• Continuing to assess human exposures including environmental measurements and population based human biomonitoring

• Reaching out to diverse groups and educating them about reducing exposures from contami-nated fish and local animal products

• Promoting a diet lower in fat

Currently, there is no consensus on appropriate state and local agency roles to reduce dioxin exposures and risks. The California Department of Health Ser-vices (CDHS) recommends that a strategic plan to monitor and reduce dioxins in California be devel-oped through broad input from local and state health agencies, community representatives, and legal experts.

DioxinsTechnical Information for California Health Officials

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Scientific evidence that dioxins are toxic to humans is increasing. Concerned resi-dents are proposing local dioxin pollu-tion prevention efforts. Health officials may be asked to support these efforts and inform the public about potentially elevated exposures. To assist health offi-cials, this document provides a review of: 1) recent scientific findings and assess-ments on sources, environmental fate, and health effects of dioxins; 2) poten-tial dioxin sources and exposures to California communities; and 3) national, state, and local risk reduction efforts.

I. Background: Recent Scientific Findings and AssessmentsOver 4,000 research articles on dioxins have been published since the 1980s. The United States Envi-ronmental Protection Agency (U.S. EPA) (1,2) and the WHO (3-6) have reviewed this research and assessed the potential health impacts of dioxins. Although the U.S. EPA planned to finalize their docu-ment in 2002 (7), their document is currently a draft. The following is a synopsis of the WHO reviews and other pertinent scientific literature.

Dioxin-like chemicals: the WHO definitionDioxin (2,3,7,8-tetrachlorodibenzo- p -dioxin or TCDD) is a member of a family of poly-halogenated aromatic hydrocarbons (PHAH). TCDD binds with an intracellular protein, the aryl hydrocarbon receptor (the Ah receptor), found in human tissues (8). The combined structure crosses into the cell nucleus and reacts with DNA, which induces a wide range of toxic responses. The WHO (3) has defined other chemicals as “dioxin-like” if they share four proper-ties with dioxin:

• similar chemical structure to dioxin

• common biochemical mechanism, binding with the Ah receptor

• similar “dioxin-like” toxic response initiated

• environmental and biological persistence

There are 29 WHO defined “dioxin-like” chemicals within three chemical classes:

2,3,7,8-chlorinated dibenzo- p -dioxins (PCDDs)

Cl

Cl

Cl

Cl

O

O

TCDD (shown) is chlorinated on the 2,3,7,8 positions of the dibenzo rings. TCDD has the highest affinity for the Ah receptor. Six of 75 other polychlorinated dibenzo-p-dioxins have 2,3,7,8 chlorination and additional chlorine atoms on the dibenzo rings.

2,3,7,8-chlorinated dibenzofurans (PCDFs)

Cl

Cl

Cl

Cl

O

2,3,7,8-tetrachlorodibenzofuran (shown) has the same chemical structure as dioxin except the benzene rings are connected by one oxygen atom instead of two. Nine of 135 other polychlorinated dibenzofurans have 2,3,7,8 chlorination with addi-tional chlorine atoms on the dibenzo rings.

Coplanar polychlorinated biphenyls (PCBs)

Cl

Cl

Cl

Cl

PCBs are a series of 209 persistent chemicals with a chlorinated biphenyl structure. Twelve of these (the non-ortho and mono ortho polychlorinated PCBs) have recently been shown to have dioxin-like prop-erties, albeit at lower potency.

These 29 chemicals are collectively referred to as “dioxins” or “dioxin-like.” In this document, “TCDD” is used to refer to 2,3,7,8-tetrachlorodibenzo- p -dioxin alone. The 29 chemicals have different toxic potentials. Concentrations of the 29 chemicals are generally toxicologically weighted and summed into one concentration, termed the International TCDD Equivalency (ITEQ) (Table 1) (3).

Not included in the 29 dioxins are other PHAHs that also bind with the Ah receptor. Some of the other

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The International Toxic Equivalency (ITEQ)Dioxins are usually present as mixtures. Table 1 provides WHO toxicological factors for each dioxin based on the ability to react with the Ah receptor and to give a dioxin-like toxic response in laboratory animals. The highly chlorinated dioxins and furans and most PCBs have factors 100- to 10,000-fold less than TCDD. These factors are used to weight the dif-ferent concentrations of the 29 dioxins and sum into a single relative concentration, the ITEQ concentra-tion. An ITEQ concentration is considered equiva-lent to a TCDD concentration and is used universally to report dioxin concentrations (3).

Only recently have PCBs been assigned ITEQ weights. When comparing concentrations between studies, whether PCBs are included in the ITEQ concentration should be noted. In this docu-ment, when ITEQ values do not include the PCBs and only include the PCDDs and PCDFs, the ITEQ value is noted as ITEQ

DF.

Sources of dioxinsDioxins are unwanted byproducts and contaminants of combustion processes and chemical manufactur-ing. Different sources contain different dioxins.

Chlorinated Organics

In the past, dioxins came primarily from produc-tion and use of chlorinated organics (5) including the pesticide, Agent Orange, PCBs, and the wood

PHAHs (polybrominated dioxins and furans) have toxic responses similar to dioxin, but the toxicologi-cal database is too limited for classification (3).

Dioxins are included in two broader classes of com-pounds, “persistent organic pollutants” or POPs, and “endocrine disruptors”(4).

Figure 1. Time-trends of total PCDDs/PCDFs inSediment, Beaver Lake, Olympic Penninsula, WA

180

160

140

120

100

80

60

40

20

01884 1897 1909 1921 1932 1946 1955 1964 1974

Data from Cleverly et al. 1996 (10)

Res

idu

e Le

vels

(pg

/g) o

f PC

DD

s an

d P

CD

Fs

Table 1: ITEQ toxicological factors for dioxin-like compounds.

ITEQ Factor PCDD, PCDF, or PCB*

1 2,3,7,8-TCDD1,2,3,7,8-PnCDD

0.5 2,3,4,7,8-PnCDF

0.1 2,3,7,8-TCDF1,2,3,4,7,8-HxCDD1,2,3,6,7,8-HxCDD1,2,3,7,8,9-HxCDD1,2,3,4,7,8-HxCDF1,2,3,6,7,8-HxCDF1,2,3,7,8,9-HxCDF2,3,4,6,7,8-HxCDFPCB 126

0.05 1,2,3,7,8 PnCDF

0.01 1,2,3,4,6,7,8-HpCDD1,2,3,4,6,7,8-HpCDF1,2,3,4,7,8,9-HpCDFPCB 169

0.0005 PCB 114PCB 156PCB 157

0.0001 OCDDOCDFPCB 77PCB 81PCB 105PCB 118PCB 123PCB 189

0.00001 PCB 167

PCDD = polychlorinated dibenzo- p -dioxinsPCDF = polychlorinated dibenzofurans*PCB = polychlorinated biphenyl (IUPAC identification)TCDD = tetrachlorodibenzo- p -dioxinPnCDD = pentachlorodibenzo- p -dioxinHxCDD = hexachlorodibenzo- p -dioxinHpCDD = heptachlorodibenzo- p -dioxinOCDD = octachlorodibenzo- p -dioxinTCDF = tetrachlorodibenzofuranPnCDF = pentachlorodibenzofuranHxCDF = hexachlorodibenzofuranHpCDF = heptachlorodibenzofuranOCDF=octachlorodibenzofuran.

Data from Van den Berg et al. 1998 (3)

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preservative pentachlorophenol (PCP) used on tele-phone poles and other wood products (9). Analysis of sediment cores throughout the United States sug-gests that dioxin deposition substantially increased between the 1930s and 1970s (10) (Figure 1).

Since the 1970s, many of the contaminated chemi-cals have been banned in the U.S. (e.g., PCBs and Agent Orange), or the use has been dramatically reduced (e.g., PCP) (9). However, dioxin contamina-tion has been detected in many other manufactur-ing processes including polyvinyl chloride (PVC, a common plastic) and textile dyes. Dioxins in dyes may be removed during household washing and concentrated in sewage sludge. 2,4-D, one of the top residential and commercial agricultural herbi-cides used in the U.S., and potentially other chlori-

nated pesticides, such as chlorthal-diethyl (dacthal), are contaminated with dioxins, albeit at much lower levels than that found in the older pesticides such as Agent Orange (5).

Incineration Facilities

Municipal and medical waste incineration and pri-mary and secondary copper smelting are the largest estimated industrial sources. However, the chemical mechanisms of dioxin formation are not completely understood. Factors that promote dioxin formation include: a chlorine source (in particular PVC, but also other chlorine sources such as the chloroparafins in waste oils); low combustion temperatures (250˚–450˚ C); poorly controlled combustion; and the presence of metal catalysts, primarily copper (5).

0 200 400 600 800 1000 1200 1400 1600 1800 2000 2200 2400 2600 2800 3000 3200

Data from Cleverly et al, 1995 (14) (except where noted).a International Toxic Equivalent (see Table 1).b Lower estimate from Winters, et al 1999 (12)c 2 – 40 houses burning trash in a representative daily burn are estimated to emit as much dioxins in a day as a modern municipal waste incinerator

in a day. Lemieux et al, 1995 (11). Emissions, therefore, set equal to municipal solid waste incineration.d Amount in 2,4-D used in one year. Data from UN Env Program, 1999 (5)

Figure 2. Estimated dioxin emissions in the U.S. from industrial and area sources, 1995.

(1,000)

(600)

(500)

(200)

(70)

(30)

(20)

(20)

(10)

(6)

(6)

(2)

(.1)

(.1)

(3,000)

(1,000)

(200)

(200)

(60)

(60)

(40)

(20)

(1)

Grams ITEQDFa/year

Industrial Sources

Municipal solid waste (air)

Secondary metal smelting/refining (air)

Medical waste incineration (air)

Cement kilns (hazardous waste burning) (air)

Industrial coal combustion (air)

Industrial wood combustion (air)

Bleached chemical wood pulp and paper mills (water, land)

Cement kilns (non hazardous waste burning) (air)

EDC/vinyl chloride manufacturing (air)

Hazardous waste incineration (air)

Sewage sludge incineration (air)

Kraft recovery broilers (air)

Crematoria (air)

Tire combustion (air)

Area Sources

PCP-treated wood, e.g., telephone poles (air, soil)b

Backyard trash burning (air)c

Municipal wastewater sludge (land)

Forest/brush, straw fires (air)

Wood combustion: residential (air)

Vehicle fuel: diesel (air)

Vehicle fuel: leaded and unleaded (air)

2,4-D (agricultural and domestic herbicide) (in product used)d

Cigarette combustion (air)

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“Area” sources

Individual sources that emit trace amounts (e.g., vehicles) may have global impact (5). Recently, backyard trash burning, where PVC is incinerated, has been estimated to release substantial amounts (11). Dioxins are estimated to be released to air and soil from PCP-treated wood, notably most tele-phone poles (12). Reused or recycled PCP-treated wood products may also have emissions (9,12).

Emission estimates

Source emission estimates are listed in Figure 2. Sources and emissions are uncertain as only an estimated 10 percent of potental sources have been tested (5). For example, as a possible con-sequence of thermal geologic processes, dioxins were recently found in mined clay products used in animal feeds and other products (13). With addi-tional testing, new sources may be discovered and emission estimates may change.

Persistence of dioxinsDioxins are non-polar, water insoluble, and stable in the environment. Their half-life in soil is more than a decade (4,15). They travel far in the atmosphere due to their tendency to adhere to soil particles and to re-suspend. Dioxins concentrate in urban runoff and sediments. Facility emissions in Florida and Mexico are estimated to travel to the northern United States and the Arctic (16). Trace amounts of dioxins have been detected in air, water, and soil in remote places. Insects, wildlife, fish, and farm animals everywhere may pick up dioxins as they eat or forage (15).

Human intake and storageDioxins are extremely lipid soluble, allowing accu-mulation in the food chain. Over 90 percent of adult human daily intake of dioxins is estimated to be from fat in fish and animal products (Figure 3).

National testing of commercial food products (17,18) has shown:

• animal products with high fat content (e.g., butter) contain the highest levels

• fresh water fish contain higher levels than ocean fish

• vegetables and olive oil contain levels almost exclusively below detection limits

In most of these foods, PCDDs, PCDFs, and PCBs each make up about a third of the fraction of the

ITEQ. When levels are combined with food surveys of consumption, estimated intake for U.S. popula-tions is 2–6 pg ITEQ /kg body weight/day for adults and children, respectively (17). Elevated levels have also been found in backyard animal produce raised near industrial dioxin point sources (19) and follow-ing incidents of feed contamination (13).

Once inside the human body, there are few meta-bolic pathways for dioxins and they become stored in fat. The estimated human half-lives for the vari-ous dioxins ranges from 4 to 20 years. Dioxins cross the placenta. The average body burden in the U.S. population is estimated at 36–58 pg ITEQ/g fat or parts per trillion (ppt) (8).

Dioxins are stored in the fat of breast milk (15). Studies in the Netherlands suggest that breast-fed infants have a 50-fold higher daily dioxin intake than adults after adjusting for body weight. Notably, short-term dietary reductions do not impact dioxin levels in breast milk. Nonetheless, the benefits of breast-feeding exceed the potential health risk from dioxins (20).

Health effectsBiochemical and cellular effects

Numerous laboratory studies have characterized the biochemical mechanisms and cellular effects. Dioxins cross the cell membrane, bind to the Ah receptor, (a putative protein product of a gene locus designated Ah), cross into the nucleus, and bind with

Figure 3. Estimated intake of dioxins by exposureroute.

1.5

1.0

0.5

0

Data from: World Health Organization (7)Schecter et al. 2001 (17)

Esti

mat

ed D

ioxi

n In

take

(pg

/kg

/day

) 1.45

0.18

0.060.00007

Animal FoodProducts

Fish Air Water

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a second protein (the Ah receptor nuclear translo-cator), which then binds with multiple elements on DNA. Binding to DNA activates the reading of genes which initiates biochemical and cellular changes including changes in the activity of enzymes, cytokines (regulators of cell division), growth factors, and hormones. Dioxins induce cell proliferation and differentiation in many tissues (8) (Figure 4).

Effects on experimental animals

Multiple effects are possible as a consequence of the diverse biochemical and cellular changes acti-vated by dioxins (8). Experimental animals die from a pronounced wasting syndrome. A wide range of effects in multiple mammalian species have also been documented, including:

• carcinogenicity

• reproductive and developmental abnormalities

• liver damage

• endocrine system disruption

• weakened immune response

• death

Human effects

The Ah receptor and associated Ah proteins are present in humans. Biochemical alterations, such as induction of liver enzymes, have been documented in humans and other biochemical alterations, such as regulators of cell division (cytokines) in primates (8).

There is now human evidence of the carcinogenic effects of dioxins. Four cohort studies (21) of those exposed while working at herbicide manufacturing plants, and one study of Italian communities exposed to an accidental release to ambient air (22), docu-ment an increase in all cancers following exposure to TCDD. For exposure to other dioxins, epidemiologi-cal studies of occupational cohorts in 12 countries suggest a similar increase in overall cancer risk (23). Among U.S. subpopulations with elevated exposures (frequent fish consumers and consumers of backyard animal produce living near dioxin sources) blood levels are equal to levels among workers with the lowest observed increased cancer risk (24).

For the wide range of other outcomes observed in animals, exhaustive epidemiological studies have

Figure 4. Biochemical mechanism of dioxin-initiated toxic response.

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not been conducted. TCDD poisoning episodes have demonstrated the skin condition known as chloracne years after exposure (25). Positive asso-ciations have been described between measured body burdens and a range of outcomes including:

• hormonal alterations (22) and sexual develop-ment (26)

• diabetes (27)

• neuro-developmental delays (28,29)

• cardiovascular (21)

• immune dysfunction (30)

Many of these studies reflect exposures to different dioxins, not just TCDD, and some suggest associa-tions at or slightly above background body burden levels (26,28,30). Nevertheless, definitive causal links with human dioxin exposures and these outcomes have not been established.

Risk assessmentsMultiple government agencies have reviewed the laboratory and human evidence and estimated the health risks of dioxins (Table 2). All of these assess-ments take a prudent public health protective approach assuming that the common biochemical mechanisms, laboratory animal studies, and tenta-tive human studies provide sufficient evidence of the potential for a range of human health effects.

The recent assessments by U.S. EPA and WHO provide cancer and non-cancer risk estimates, respectively. The external scientific review panel for the U.S. EPA 2000 assessment has agreed with the estimate of a cancer risk of one in 1,000 for the gen-eral population from background dioxin exposures (2). This cancer risk is higher than the one in a million cancer risk at which public health action to reduce air and water exposures has been taken (33,34).

Table 2: International, federal, and state health assessments by reporting year

Year Agency Type of Assessment Conclusion or Action

1985 California Air Resources Board (CARB)

Cancer risk assessment (31) Listed dioxins as toxic air contaminants.

1988 Prop 65 Cancer and reproductive toxicity Listed dioxins as carcinogens and reproductive toxins.

1994 U.S. EPA Extensive health risk assessment Draft document.

1998 WHO Calculated a tolerable daily intake (TDI) for non-cancer effects

Establishes a TDI of 1-4 pg ITEQ/kg body weight per day (6).

2000 The International Agency for Research on Cancer (IARC)

Cancer review TCDD is a human carcinogen (21).

2000 U.S. EPA Reassessment: extensive review of all literature on sources, environmental fate, and health risk assessment

Draft document. TCDD is a human carcinogen with a cancer risk of 1 in 1000 for the general population from background dioxin exposures (1).

2000 External review panel for U.S. EPA

Reviews U.S. EPA 2000 document Agreed with conclusions of 2000 U.S. EPA document (2).

2001 CalEPA- Office of Environmental Health Hazard Assessment

Evaluation of susceptability to children mandated under the Children’s Environmental Health Protection Act (Senate Bill 25, Escutia, chaptered 1999)

Declared dioxins one of five toxic air contaminants that may cause children and infants to be particularly susceptable to illness (32).

2002 U.S. General Accounting Office

Compares WHO and U.S. EPA risk assessment methodology and conclusions

U.S. EPA and WHO differ on methodology. However, both conclude that dioxins can adversely affect human health at lower levels than previously thought (7).

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For non-cancer effects, WHO has recommended a tolerable daily intake (TDI). The TDI is a reference level below which the WHO regards as safe. The TDI was calculated from the lowest observed effect levels for the most sensitive outcomes (neuro-developmental and reproductive effects and endo-metriosis) in laboratory animals and then applying a ten-fold uncertainty factor. WHO estimated that dietary intakes for industrialized background populations (2–6 pg ITEQ/kg body weight per day), including the U.S., are equal to or above the TDI intake. Thus, current dietary levels are approaching levels of public health concern (6).

II. Dioxins in CaliforniaCalifornia has different dioxin sources than those described nationally. In this section, California sources and potential exposures are reviewed.

Stationary industrial point sourcesNationally, medical and municipal waste incin-erators have been identified as major sources of dioxins (Figure 2). In 1990, toxic air contaminant regulations were initiated requiring California medical waste incinerators to achieve a 99 percent reduction in dioxin emissions (35). Thereafter, the number of medical waste incinerators in California fell from about 150 to less than 10. Currently, there are only three small municipal waste burners in California. Other industrial point sources identified nationally, including PCP wood treatment facilities and secondary copper recovery facilities, no longer operate in California or have significantly reduced operations.

Operators of stationary industrial facilities in Cali-fornia are required to report air emissions of dioxins to their local air district. In 1997, the California Air Resources Board (CARB) used these reports (35) to identify the following sources:

• Sanitary services (thermal and combustion pro-cesses)

• Manufacturers of medical instruments and sup-plies

• Manufacturers of cement and hydraulics products

• Manufacturers of miscellaneous plastic products

• Sawmills and planing mills

Recent testing in California has also revealed dioxin air emissions from refineries (36). Facilities may also have releases to land and water (Figure 2). Never-theless, many other types of industrial point sources identified nationally have not been adequately tested anywhere else in the U.S. (5).

Potential exposures near industrial sources

Occupational Exposures: Workers have been exposed to dioxins at the types of facilities report-ing emissions in California (37).

Accidental industrial fires and releases: Accidental fires of dioxin-contaminated chemicals have oc-curred in California (19). The significance of indus-trial fires or accidents depends on the process at the facility and the presence of chlorinated organic chemicals. For example, testing of source material from a fire at a tire facility in the Central Valley did not reveal significant dioxin contamination.

Locally caught fish: Contamination in fish (primarily, PCBs) near a few hazardous waste facilities has war-ranted fish advisories (38).

Backyard animal products: In three areas in Cali-fornia near former industrial facilities, dioxin levels in products (primarily chicken eggs) from animals that forage on backyard soil year-round have been elevated above health concern levels. Levels in eggs from these three areas are also above levels in eggs from backyard foraging chickens raised in a compa-rable rural area with no known dioxin emitting indus-trial facilities. Residents who had eaten these elevated products for many years had higher body burdens (24). Consumption advisories for eggs from forag-ing chickens were issued in these three areas (39). Whether animal product contamination is present near existing or former municipal and medical waste incinerators in California has not been studied.

“Area” sourcesIn the U.S., about 65 percent of estimated dioxin emissions come from area sources, rank ordered in Table 2. These estimates may not be representative of California. Nevertheless, in California, area sources probably contribute to the global burden of dioxins. These include:

Backyard burning of trash, PCP treated wood, and metal recovery: In some rural areas of Cali-fornia, backyard burning of trash is allowed. Open

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burning of copper wire where plastics are burned off to recover the copper or other metal materials is easy and profitable. In remote areas of California, restrictions may be difficult to enforce.

PCP-treated wood emissions: PCP-treated tele-phone poles are ubiquitous in California. In addition, reused or recycled products are used in California.

Municipal wastewater sludge and fertilizers: In 1998, 460,000 dry tons of sewage sludge were applied to agricultural land in 26 California counties (40). Levels in sludge (50 ppt ITEQ) (41) are above soil levels (1–2 ppt ITEQ

DF) estimated for foraging

chickens to accumulate significant amounts in eggs (19). Monitoring also suggests that application of sewage sludge increases dioxin concentrations of soil (42).

Pesticides: Millions of pounds of the herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) are used in Cali-fornia agriculture annually. National 2,4-D use data suggests that agricultural use is only slightly greater than non-agricultural use (43).

Other probable sources: Forest fires, wood burn-ing, agricultural burning, diesel, and vehicle exhaust contribute (Figure 2) (5). Area sources which have not been quantified on a national level, but are probable in California, include structural and vehicle fires where there is burning of plastics and metals or PCP-treated wood. Fires of PCB transformers at office buildings in California have also occurred.

Environmental concentrations in CaliforniaBoth area and stationary industrial point sources contribute to environmental concentrations. Moni-toring studies undertaken to measure background environmental concentrations in California are pre-sented below.

Air: Dioxin levels in Los Angeles and Fresno (44) have been similar to ambient urban air values nationwide (45). In Fresno, the pattern of dioxin con-centrations was representative of wood burning, which was considered the primary source. CARB developed an ambient air monitoring program for the San Francisco Bay Area and Los Angeles, which began in the summer, 2001.

Drinking water: Dioxins, which are hydrophobic and adhere to particulate matter, should settle or

be removed from drinking water. Water providers may waive testing under certain conditions (46). Since the CDHS drinking water standard for TCDD (30 parts per quadrillion (ppq or pg/L) TCDD) was established, a large number (1,100) of California drinking water sources have been tested. No con-firmed detections of TCDD have been reported, with a reporting limit (5 ppq) below the standard.

Ambient surface water and storm water runoff: In 1984, the U.S. EPA promulgated a guideline of 0.013 ppq TCDD for ambient surface water (thereby indus-trial effulent). Noteably, this U.S. EPA guideline is much lower than the CDHS drinking water standard (30 ppq). U.S. EPA intends to regulate the guideline as ITEQ when the reassessment is finalized (34). In the greater San Francisco Bay Area, dioxins (measured as ITEQ) have been detected in filtered storm water outfall at levels above the surface water guideline (average levels between 10–25 ppq ITEQ) (47).

Commercial food products: National samples include California (17) or the Northwest (48). How-ever, the number of samples from California is too small to state whether levels in food produced in California are different from national levels.

Locally caught fish: Dioxins have been detected in fish from the large bays of California’s coast. Most of these areas have fish advisories. These advisories, however, are in large part driven by the now banned dioxin-like PCBs (49).

Backyard animal products:

Rural areas: Eggs from chickens raised on soil in a California rural area with no known dioxin sources had contamination below levels war-ranting consumption advice, but about seven-fold higher than commercial eggs (19). These results suggest that eggs from foraging chick-ens in rural areas of California may be a source of slightly elevated human exposure.

Suburban or urban areas: The range of soil levels associated with elevated animal product con-tamination warranting consumption advice included low levels (as low as 1–2 ppt ITEQ

DF, in

soil). These low levels are in the range reported nationally for urban areas (19). In California, soil levels in suburban or more urbanized agricul-tural areas, where people may raise chickens, are unknown. However, a California Depart-ment of Food and Agriculture study of Califor-nia farmland soils is in progress.

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Human biological monitoringBlood or fat: Among two separate groups of San Francisco Bay Area residents, estimated body burdens in 1988 and 1998 were no different from nationwide urban estimates. 1998 levels were lower than 1988 levels (50). Additionally, a small group of residents (n=9), from a rural area in California with no known dioxin emitting facilities, who did not consume backyard animal products, had lower levels than nationwide urban residents suggesting urban/rural differences (24).

Breast milk: In the U.S., a few breast milk samples have been collected (17) including a few from Stock-ton, California, which were low compared to values from Europe (50).

III. Reducing RisksA group of over 100 countries, including the U.S., with technical support from WHO, have negotiated a treaty to ban and/or severely restrict the release of 12 persistent organic pollutants, including diox-ins. Except for dioxins, which are byproducts and are more difficult to control, the others have been banned in the U.S. For dioxins, the goal of the treaty is “their continuing minimization and, where fea-sible, ultimate elimination” (51). The American Public Health Association and the California Medical Asso-ciation have issued supporting policy statements. Although in California, and nationally, there are significant data gaps in knowledge on sources and

environmental levels, regulatory agencies, industry, and other scientists have undertaken numerous efforts toward risk reduction. Local officials may choose to support or implement these efforts.

Primary prevention is source reductionSource reduction includes engineering changes to reduce facility emissions and consumer product contamination, use reduction of contaminated prod-ucts, and separation of products involved in dioxin formation from incineration feedstreams. Testing of sources or emissions are also first steps toward pollu-tion reduction. Specific efforts have included:

National efforts

• The U.S. EPA has taken action to reduce emis-sions from facilities including mandated controls on municipal, medical, and hazardous waste incinerators. Other regulations include pulp and paper effluent guidelines (52). The U.S. EPA has also developed a repository of testing of source emissions conducted by federal and state agen-cies, trade associations, and others (53).

• The American Public Health Association has passed a resolution calling for the phase out of PVC materials (54).

• To eliminate PVC, scientists have suggested tools such as “green” purchasing for hospitals (55).

• The U.S. Department of Agriculture (USDA) eliminated use of dioxin-contaminated animal feed (13).

When are local biological monitoring studies appropriate?

CDHS has conducted local dioxin biological monitoring studies to verify in specific contamination incidents that elevated environmental exposures lead to elevated body burdens (24). Such studies require:

• measured elevated environmental exposures

• community informed consent (i.e., community representatives agreeing that there is benefit to the study)

• human subjects panel review (a process that requires 3–6 months and a generalized benefit to society)

• special funds as chemical analysis of dioxins is expensive ($1,500–2,000 per sample)

If individual residents request biological monitoring, possible local health department efforts include edu-cational efforts and informal exposure histories (e.g., historical diet and occupational exposures). There is no method for removing dioxins from humans. Biological monitoring can only potentially verify elevated exposure. Further, the ability to link body burdens to specific exposures is limited. CDHS can provide con-sultation in evaluating potential high exposures.

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State efforts

• Over the next two years, CARB will be testing air emissions of 12 stationary facilities, possibly including medical waste incinerators, catalytic oxidizers (a thermal process used in chemical cleanup), refineries, drum reconditioners, land-fills, and secondary metal recovery facilities.

• CARB is adopting regulations which will severely reduce backyard burning of house-hold garbage, and eliminate burning of plastics in 2004 (56).

• California’s State Water Resources Control Board (SWRCB) has prepared statewide General Waste Discharge Requirements for the application of sewage sludge to farmland, including some restrictions on applications (57).

• CARB has classified dioxins as one of the 42 toxic compounds in diesel exhaust. A diesel risk reduction program has been initiated (58).

• Reductions in agricultural burning would reduce re-suspension of dioxins. In California, a state-wide smoke management task force exists to encourage techniques to minimize smoke (59).

Local efforts

For facilities that report dioxin air emissions to local air districts or report land/water emissions to other agencies county health officials may:

• Track any regulatory agency or industry efforts to reduce emissions. Reporting regulations involve multiple agencies. A report from Santa Clara County (60) provides a model for access-ing datasets.

• Review emergency response procedures; con-sider inclusion of dioxin testing following fires or other thermal accidents involving dioxin contaminated products or chemicals.

Twenty-nine of 35 air districts in California pro-hibit backyard burning of any garbage (56).

Several cities in the San Francisco Bay Area have adopted resolutions to “eliminate or stop” dioxins. Some options under consideration include elimi-nation of medical PVC use, alternatives to diesel engines and non-PVC plastic use, use of non-wood utility poles, and restrictions on use of 2,4-D (61).

Sixteen California counties and/or towns have restrictions, bans, or ordinances on land applica-tion of sludge. Other counties have appointed task forces to investigate the practice (62).

Secondary prevention is human exposure reductionSecondary prevention efforts reduce human expo-sure but do not lower the global ecosystem burden of dioxin. Such efforts offer an immediate way for sub-populations to reduce dietary intake. Most notably:

Eat a diet low in animal fats: Eating a diet low in animal fats is recommended by Federal Dietary Guidelines (63) and may lower exposures to diox-ins. However, the WHO has noted that given the long biological half-life of dioxins, the ability of consumers to mitigate their own dioxin burden is limited.

Adhere to local fish advisories: Adherence to advisories in the large coastal bays of California (49) and near former industrial facilities (38) will reduce human intake.

Reduce exposures from backyard animal products:• Near stationary industrial point sources: For cer-

tain facilities that have released dioxins in the past (i.e., former wood treatment facilities, sec-ondary metal recovery facilities, medical waste incinerators) and for facilities that report air emissions to their local air district, local health officials may:– Identify and focus educational efforts on local

sub-populations with potentially elevated exposures (e.g., subsistence fishers and back-yard egg producers).

– Among such local sub-populations, ask responding agencies to test fish and locally produced animal foods. Such testing would confirm whether dioxin concentrations are elevated.

• Throughout California: For those who are con-cerned about dioxin exposures from products raised in backyards anywhere in California, local health officials may recommend:– Changes in husbandry practices that reduce

contact with soil, including raising chickens in cages above soil. This practice is also rec-ommended by state agricultural agencies to reduce the spread of infectious diseases between birds.

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Tracking progressEfforts to reduce risks and exposures may be evaluated by source, environmental, and biologi-cal monitoring. For example, recent data suggests that national levels in cow milk have declined since the mid-1980s when restrictions on munici-pal solid waste incinerators were instituted (48). In the San Francisco Bay, a 4- to 7-fold decline in PCB levels in mussels in the last 15 years has been observed (49). Because sources and emissions of dioxins are uncertain, such monitoring may be critical to understanding whether pollution reduc-tion efforts are effective.

Some health officials have expressed interest in human biological monitoring. Systematic sampling has suggested a decline in human dioxin body bur-dens and breast milk in industrialized countries (15). CDHS supports national efforts by federal agencies to estimate background dioxin levels in blood and body fat (64). Researchers have also argued that a breast milk monitoring program is necessary to understand exposures to a vulnerable population

(65). However, because dioxins are persistent global pollutants, whether human biological monitoring can effectively monitor local pollution reduction efforts is open to debate. Biological monitoring studies described for California herein do not sug-gest differences with the rest of the U.S. but do very tentatively suggest intriguing temporal changes and differences within the state. Further nationwide monitoring efforts (66) are currently in progress. CDHS will evaluate the California-specific results when results become available.

Future effortsU.S. EPA plans to release its comprehensive reas-sessment and to then use it to develop a national risk management strategy (7). However, there is no consensus on appropriate state and local agency roles to reduce dioxin exposures and risks. CDHS recommends that a strategic plan to monitor and reduce dioxins in California be developed through broad input from local and state health agencies, community representatives, and legal experts.

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AcronymsCARB: California Air Resources Board

CDHS: California Department of Health Services

2,4,-D: 2,4-dichlorophenoxyacetic acid

EHIB: Environmental Health Investigations Branch

IARC: International Agency for Research on Cancer

ITEQ: International Toxic Equivalency (includes PCDDs, PCDFs and PCBs,)

ITEQDF

: International Toxic Equivalency (PCDDs, PCDFs only)

L: liter

ng: nanogram

PCBs: polychlorinated biphenyls

PCDDs: 2,3,7,8-chlorinated dibenzo- p -dioxins

PCDFs: 2,3,7,8-chlorinated dibenzofurans

PCP: pentachlorophenol

PHAH: poly-halogenated aromatic hydrocarbons

pg: picogram

POP: persistent organic pollutants

ppb: parts per billion

ppt: parts per trillion

PVC: polyvinyl chloride

SWRCB: State Water Resources Control Board

TCDD: 2,3,7,8-tetrachlorodibenzo- p -dioxin

TDI: Tolerable daily intake

WHO: World Health Organization

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Gray DavisGovernor

State of California

Grantland JohnsonSecretary

Health and Human Services Agency

Diana M. Bontá, R.N., Dr.P.H.Director

Department of Health Services

CaliforniaDepartment ofHealth Services