- Email: [email protected]
Asbestos-Contaminated Drinking Water
Asbestos-Contaminated Drinking Water James S. Webber New York State Department of Health
I. II. III. IV. V.
Mineralogy and History Occurrence Health Hazards Analysis Control
Glossary Asbestosis Nonmalignant, dose-related, lung dis ease (pneumoconiosis) marked by interstitial fi brosis and reduced pulmonary efficiency. Aspect ratio Fiber length divided by fiber width. Mesothelioma Rare malignant tumor of the body linings (pleura, peritoneum, or pericardium) which grows diffusely as a thick sheet covering the viscera. Micrometer (μιη) One thousandth of a millimeter. + pH Negative logarithm (base 10) of the H con centration in water. Water with pH <7 is con sidered acidic and water with pH > 7 is considered alkaline. Standardized mortality ratio (SMR) Ratio of mor tality in a study group divided by the expected mortality from a control group. The ratio is usu ally expressed as percentile, with values less than 100 indicating lowered mortality among the study group and values greater than 100 indicating higher mortality among the study group. Transmigration Ability of particles to pass from the digestive tract through the intestinal wall and into the circulatory system.
ASBESTOS is α collective term that describes natu rally occurring hydrated silicate minerals that break into fibers. Asbestos is naturally present in some water bodies but its accelerated use in the twentieth
century has increased its concentration in many other water systems. Although ingested asbestos does not appear to be as hazardous as airborne asbestos, some ingested asbestos undoubtedly reaches the bloodstream and a few studies have revealed a possible link between this migration and tumors at areas remote from the pulmonary or di gestive systems. Some epidemiologic studies of pop ulations drinking asbestos-contaminated water have detected increased gastrointestinal cancer. A prudent course of action is to minimize asbestoscontamination in drinking water through proven, cost-effective methods.
I. Mineralogy
and History
A. Semantics, Mineralogy, and Properties The ancient Greeks called these flexible, fireresistant minerals ctaßsaros, meaning inextin guishable or unquenchable. Asbestos characteris tically breaks into very thin fibers, often as narrow as 0.025 μιη in diameter, which have high resistance to heat and have enormous tensile strength. Defini tions for asbestos have changed over the centuries as new varieties have been identified and as classifi cation systems have evolved. Controversy over pre cise definitions continue today because of differ ences in regulatory and commercial perspectives. Six mineral types are currently recognized as as bestos (Table I). The sole serpentine variety, chrysotile, is the most common type of asbestos, ac counting for more than 90% of worldwide production. Chrysotile is the most flexible of the asbestos types and is the most vulnerable to leaching by acids. Its structure is unique among asbestos varieties—a magnesium hydroxide layer overlies a
Handbook of Hazardous Materials Copyright © 1993 by Academic Press, Inc. All rights of reproduction in any form reserved.
23
30
Asbestos-Contaminated Drinking Water
Table I Characteristics of Asbestos Minerals Mineral type
Variety
Chemical formula
Serpentine
Chrysotile
Mg 3(Si 20 5)(OH) 4
Amphibole
Amosite (grunerite)
(Fe,Mg) 7(Si 80 2 2)(OH) 2
Crocidolite (riebeckite)
Na 2Fe 5(Si 80 2 2)(OH) 2
Anthophyllite
(Mg,Fe) 7(Si 80 2 2)(OH) 2
Tremolite
Ca 2Mg 5(Si 80 2 2)(OH) 2
Actinolite
Ca 2(Mg,Fe) 5(Si 80 2 2)(OH) 2
silicate layer, forming an elongated scroll. The five amphibole asbestos types have more typical struc ture, with double-chain silicates sandwiching a cation (Fe, Mg, Na, or Ca) layer. Crocidolite is an iron- and sodium-rich riebeckite asbestos that has higher tensile strength than any other asbestos type. Amosite, an iron- and magnesium-rich grunerite fi ber, is highly resistant to leaching. Anthophyllite is a magnesium-rich amphibole that has the highest fu sion point. Tremolite and actinolite are in a calciumiron replacement series and are of little commercial significance.
0. History of Asbestos and Humans Although asbestos was woven into fireproof cloth by ancient Greeks and used as lamp wicks in medieval times, its utilization was fairly limited until the be ginning of the twentieth century. At about that time, people began to recognize the diverse technological applications of the unique properties of asbestos, namely its thermal and electrical resistance, tremen dous tensile strength, chemical resistance, flexibil ity, and low cost. In response to escalating de mands, asbestos production increased more than 100-fold during the first eight decades of the cen tury. Thousands of uses have been described for asbestos, ranging from sprayed-on fireproofing and insulation to brake linings, floor tiles, shingles, asbestos-cement pipes, and missile covers. An increase in disease was inevitable as the ex ploitation of asbestos accelerated during the twentieth century. In some instances, however, these elevations were not noted immediately be cause of the latency period, usually measured in decades, between the time of exposure and the man ifestation of symptoms. Asbestosis was first docu
mented around 1930 in asbestos workers and shortly thereafter, increased incidences of lung cancer were also noted. Following World War II, an alarming increase in mesothelioma, a previously rare disease, was noted not only in asbestos workers but also in persons marginally exposed to asbestos. Because these diseases were associated with inhalation of airborne asbestos fibers, increasingly stringent regu lations have been enacted during the past few de cades to reduce exposure of workers and the public to airborne fibers. Does asbestos-contaminated drinking water pose a health hazard similar to airborne asbestos? Most studies have indicated that, while there may be some health risks associated with ingestion of asbestos, the health hazards are substantially less than those posed by inhalation. This is discussed in more detail in Section III.
Occurrence
II.
A. Large-Scale
Surveys
The majority of water-supply systems in North America contain less than one million asbestos fi bers per liter (MFL). A survey of several hundred systems in the United States revealed that more than 80% had less than one MFL while only 10% had more than ten MFL (Table II). Similarly, in Canada 5% of the population receive more than one MFL while less than 1% receive more than 100 MFL. Comparable surveys in Europe have revealed simi lar patterns. Table II Distribution of Reported Asbestos Concentrations in Drinking Water from 406 Cities in 47 0 States, Puerto Rico, and the District of Columbia Highest asbestos concentration 6 (10 fibers/L)
Number of cities
Percentage
Below detectable limits
117
28.8
<1
216
53.2
1-10
33
8.1
>10
40
9.9
Total
406
100
" From Millette, J. R., Clark, P. J., Stober, J., and Rosenthal, M. (1983). Asbestos in water supplies of the United States. Envi ronmental Health Perspectives, 53, 45. Reproduced by per mission.
31
Asbestos-Contaminated Drinking Water
B. Episodes of Gross
Contamination
In spite of the generally low asbestos concentrations in public water-supply systems, there have been several instances where concentrations have been drastically elevated. While some of the highest con centrations were from non-point sources, pointsource contamination was also significant on a local ized level. 1 . Natural Erosion Some of the highest waterborne concentrations of asbestos have been measured in areas of serpentinized bedrock where erosional processes often en train chrysotile into drinking water. In eastern North America, such outcroppings have produced concen trations of more than 1000 MFL in Quebec and New foundland. Likewise, erosion of serpentinized de posits in California have generated concentrations in excess of 10,000 MFL. Further north in Washing ton State, chrysotile concentrations have exceeded 100 MFL due to erosion. Chrysotile fibers produced by natural erosion are generally small, usually less than 1 μιη in length. Elevated amphibole asbestos concentrations are rarely encountered in natural wa ters of North America. 2. Deteriorated AC Pipe Asbestos fibers are susceptible to sloughing off the inner surfaces of deteriorated AC pipes during trans mission of water. Corrosive water often accelerates this process by dissolving the cement matrix of the AC pipe. An Aggressiveness Index (A.I.) has been proposed by the American Water Works Associa
Table III
tion to predict the potential for water to corrode AC pipe. This is defined as A.I. = pH + log 1 0 [alkalinity (mg/L as CaC0 3 ) + hardness (mg/L as C a C 0 3 ) ] . Indices less than 10 are considered highly aggres sive. In a South Carolina drinking water system, corrosive water's disintegration of AC pipe was blamed for chrysotile concentrations in excess of 500 MFL. In Woodstock, New York, concentra tions of chrysotile and crocidolite in excess of 1000 MFL were attributed to long-term degradation of AC pipe by acidic water. Factors such as seasonal use, drastic changes in water pressure, and improper tapping and cutting operations can also contribute to elevated concentrations.
3. Anthropogenic Disturbances One of the most widely reported contamination epi sodes was discovered in Duluth, Minnesota during the 1970s. An iron-mining operation had been dis posing of taconite tailing wastes into western Lake Superior for two decades; amphibole fibers from these tailings eventually turned up in the unfiltered drinking water of Duluth. During times of turbu lence, concentrations would reach 600 MFL. This dumping was eventually stopped and Duluth insti tuted filtration to remove residual fibers from the drinking water. In another instance, concentrations of up to 74 MFL were blamed on an old asbestos waste pile in Kentucky.
Some Size Characteristics of Asbestos Fibers Found in Various Water Supplies
Source
Type of fiber
0
Number of fibers measured
Average length (μηι)
Average width (μτη)
Average aspect ratio
Maximum length found (μτη)
Reservoir with natural erosion (WA)
Chrysotile
289
0.8
0.034
25:1
3
Reservoir with natural erosion (CA)
Chrysotile
644
1.3
0.04
39: 1
10
Cistern with asbestos tile roof (VI)
Chrysotile
342
2.3
0.04
62: 1
25
Distribution sites from five asbestos cement pipe systems (SC, PA, FL)
Chrysotile
1440
4.3
0.044
121 : 1
80
Lake Superior (MN)
Amphibole
468
1.5
0.18
11: 1
14
α
From Millette, J. R., Clark, P. J., Pansing, M. F., and Twyman, J. D. (1980). Concentration and size of asbestos in water supplies. Environmental Health Perspectives 34, 22, Reproduced by permission.
Asbestos-Contaminated Drinking Water
32
C. Characteristics of Waterborne Asbestos As previously discussed, chrysotile is the dominant asbestos type identified in water samples. This re flects its widespread use in industry and its abun dance in nature. Chrysotile, with its unique positive surface charge, is vulnerable to attack by acids and may degrade in low-pH water systems. Amphiboles, on the other hand, are more impervious to disso lution but are rarely encountered in drinking wa ter samples. Amphiboles are often minor cocontaminants with chrysotile when deteriorated AC pipes are the asbestos source. Asbestos-like mineral fibers such as halloysite, rutile, and palygorskite have been occasionally detected in water systems but little is known about potential biological effects of ingestion of these fiber types. Asbestos fibers resulting from AC pipe or anthro pogenic activity usually have larger dimensions than fibers from natural erosion sources (Table III). Indi vidual fiber length, width, and especially mass 2 (length x width x density) are often distinctly larger from human-derived sources.
III. Health
Hazards
Although evidence that inhalation of asbestos can cause serious health problems is overwhelming, health risks posed by ingestion of asbestos are ap parently much lower.
A.
of the intestines. One drawback in relating these feed studies to ingestion of waterborne asbestos is that most animal studies were performed with much longer fibers than are normally found in asbestoscontaminated drinking water. In addition, asbestos fibers embedded in food pellets used in the animal studies may behave differently from the loose fibers characteristic in drinking water. 2. Transmigration Studies Asbestos fibers typically found in contaminated drinking water are small enough to pass through the wall of the small intestine and into the blood and lymph fluid. Most studies that have investigated this possibility have found that fibers do indeed reach the 7 circulatory system, probably at a ratio of ΙΟ" to 3 10~ of the fiber concentrations ingested. Elevated concentrations of amphibole fibers were measured in the urine of Duluth residents who had been drink ing contaminated Lake Superior water. Several studies on asbestos workers have also detected in creased asbestos levels in urine. Elevated asbestos concentrations have been detected in various tissues and organs of laboratory animals that have ingested asbestos. Many of these human and animal studies have found a preferential transmigration of small fibers (usually shorter than 2 μ,πι), the size range most common to drinking water. Some case studies of cancers of digestive and urinary organs in asbes tos workers have revealed asbestos fibers in these organs. However, a larger body of evidence with controls will have to be accumulated before defini tive linkages can be established.
Ingestion
1 . Animal Toxicity Studies Most investigations of asbestos ingestion by labora tory animals have failed to produce evidence of tox icity or consistent, reproducible, organ-specific car cinogenicity. The largest series of studies was performed by the National Toxicology Program (NTP), under the auspices of the National Institute for Environmental Health Sciences, in which large numbers of diverse rodent populations were fed a variety of asbestos types. With the exception of one study that revealed an increase in large-intestine tu mors, all other NTP studies revealed no significant health differences between experimental and con trol populations. While most other studies have sim ilarly failed to demonstrate pathogenicity of ingested asbestos (Table IV), there have been indications of induced abnormalities such as impeded permeability
3. Epidemiologic Studies a. Ecological Studies More than a dozen epidemiologic studies investi gated possible correlations between asbestoscontaminated drinking water and cancer mortality. Certain investigations have revealed statistically significant correlations with various organs and tis sues, but most have not revealed a definitive associ ation (Tables V and VI). Some of the most signifi cant studies have focused on the San Francisco Bay area, where long-term contamination of water by chrysotile has resulted from natural erosion of serpentinized bedrock. A large population and population-based cancer registries in the Bay Area have increased statistical sensitivity and enhanced meaningful analyses. Several investigations there have revealed positive correlations for combined
Species Rat
Rat
Rat
Rat
Bonser [1967]
Gross [1974]
Gibel [1976]
Cunningham [1977] 1% in diet ad libitum
0 1% in diet ad libitum
Control Chrysotile
0
Control Chrysotile
20 mg/day
Talc
0
Control 20 mg/day
10 mg/wk
Crocidolite (2 sources) Chrysotile
10 mg/wk
5 mg/wk
Crocidolite 0
10 mg/wk
Chrysotile
Control
0
Control
Crocidolite
5% in diet ad libitum
0
Control Chrysotile
0.15% in diet ad libitum
Dose
0
Crocidolite
Test material
Summary of Asbestos Ingestion Studies
Study (author [date])
Table IV
To 24 mo
0
To 24 mo
0
Life
Life
0
18 wk
0
16 wk
16 wk
16 wk
0
21 mo
0
To 78 wk
Exposure time
c
£
To 30 mo
6 24 mo
To 24 mo
702
649
441
c
To 1.5 yr
To 1.5 yr
To 1.5 yr
To 1.5 yr
To 1.5 yr
To 1.5 yr
21 mo
21 mo
To 86 wk
To 78 wk
Study duration
•0/36
'J/8
10/7
50/49
50/45
50/42
24/24
63/63
24/24
34/34
33/33
31/31
5/5
10/10
65/25
40/12
Number of animals (initial/ examined)
11
1
6
2
3
12
0
0
5
1
0
2
0
0
1
0
Number
2 Thyroid Thyroid Liver Chemodectoma jugular body
Peritoneum
Brain Pituitary Node 2 Kidney Peritoneum
Liver
Liver
Lung 4 Kidney 3 Node 4 Liver
3 Breast Thigh Node
Node
Breast
Liver
Location
c
C S
S
S C L C S
C
C
C C L C
C S L
L
C
S
Type*
(continues)
Malignant tumors
Species
Rat
Hamster
Rat
Study (author [date])
Wagner [1977]
Smith [1980]
Bonham [1980]
Table IV (Continued)
0
Control
Control
Cellulose fiber
Chrysotile
Control
Taconite tailings
Taconite tailings
Taconite tailings
Amosite
Amosite
libitum
0
ad
libitum
10% in diet
ad
10% in diet
0
libitum
50 mg/L ad
libitum
5 mg/L ad
libitum
0.5 mg/L ad
libitum
50 mg/L ad
libitum
5 mg/L ad
libitum
0.5 mg/L ad
100 mg/day
Talc
Amosite
100 mg/day
0
Dose
Chrysotile
Control
Test material
0
To 32 mo
To 32 mo
0
To 23 mo
To 23 mo
To 23 mo
To 23 mo
To 23 mo
To 23 mo
0
101 days/5 mo
101 days/5 mo
0
Exposure time
£
c
c
To 32 mo
To 32 mo
To 32 mo
To 23 mo
To 23 mo
To 23 mo
To 23 mo
To 23 mo
To 23 mo
To 23 mo
641
614
619
To 30 mo
121/115
242/197
240/189
120/120
60/60
60/60
60/60
60/60
60/60
60/60
16/16
32/32
32/32
40/32
Number of animals (initial/ Study duration examined)
3
2
4
1
0
0
1
0
3
1
0
3
3
11
Number
Colon
Colon
3 Colon Abdominal mesothelioma
Node
Uterus
2 Stomach Peritoneal mesothelioma
Lung
2 Uterus Stomach
Node Stomach Uterus
Thyroid Liver 2 Adrenal Kidney Node 5 Fat
Colon Ileum Adrenal 2 Node Bone
Location
Malignant tumors
C
c
C
L
S
C
C
S S
L S S
L S
c c c c
L S
s c
C
Type*
Rat
Rat
Rat
Ward [1980]
Ward [1980]
Hiding [1981]
100 MFL ad libitum
5,000 MFL ad libitum
100,000 MFL ad libitum
Unfiltered Duluth tapwater
Lake Superior water sediment
Taconite tailings
l/wk(SC) 10 mg 3/wk
Saline plus amosite 1 MFL ad libitum
7.4 mg/kg wk 10 mg 3/wk
Azoxymethane plus amosite
Filtered Duluth tapwater
7.4 mg/kg wk
Azoxymethane
—
1.0 mL 3/wk (gavage)
Saline Untreated
10 mg 3/wk 10 mg 3/wk
7.4 mg/kg wk 10 mg 3/wk
Azoxymethane plus chrysotile
Chrysotile
7.4 mg/kg wk 10 mg 3/wk
Azoxymethane plus amosite
Amosite
7.4 mg/kg wk
Azoxymethane'*
870
840
c
c
c
c
960
690
10 wk
10 wk
10 wk
0
10 wk
10 wk
10 wk
10 wk
10 wk
10 wk
870
c
c
c
£
840
960
690
To95wk
To95wk
To95wk
34 wk
34 wk
34 wk
34 wk
34 wk
34 wk
34 wk
30/30
22/22
30/28
28/27
50/49
50/48
50/48
21/21
21/21
21/21
21/21
21/21
21/18
21/21
3
3
4
3
17
44
39
0
0
0
0
10
10
12
Neck Chest wall Mediastinum
Lung Skin Uterus
Salivary gland Skin Uterus Mediastinum
Lung Ovary Forestomach
Ileum 16 Colon
15 Ileum 29 Colon
12 Ileum 27 Colon
4 Ileum 6 Colon
5 Ileum 7 Colon 3 Ileum 7 Colon
(continues)
S S L
C C S
C C S L
C C C
C C
C C
C C
C C
C C C C
Rat
Bolton [1982]
Life Life
840
25 mo. 25 mo. 25 mo.
250 mg/wk 250 mg/wk 250 mg/wk
0
0
Amosite Crocidolite Chrysotile
Margarine control
Control
Fat Pleural histiocytoma 2 Adrenal Plasma cell tumor 2 Adrenal Bladder Peritoneum Fat Lymphoma
1 5
4
2
22/22
24/24
23/23
Life
Life
Life
0
0
Stomach Adrenal
1 22/22
Salivary gland 2 Uterus Skin Peritoneal mesothelioma
Leukemia
Breast 2 Fibrous histiocytoma Skin Mediastinum Pleural mesothelioma
24/24
1
6
Location
5
20/20
30/30
Number
Malignant tumors
30/30
840
£
£
20 mg/day
750
Diatomaceous earth
c
c
750
300 mg/day
£
Amosite
870
870
£
Study duration
20 mg/day
Dose
Exposure time
Chrysotile/amosite
Test material
Number of animals (initial/ examined)
s
c c s
c
c s s
S
C S C
C L
C
Type*
From Condie, L. W. (1983). Review of published studies of orally administered asbestos. Environmental Health Perspectives 53,4-7. Reproduced by permission. * Type C, carcinoma; S, sarcoma, L, lymphoma. £ Mean survival time in days. d Azoxymethane given subcutaneously; saline administered by oral gavage or subcutaneously.
a
Species
(Continued)
Study (author [date])
Table IV
(+-) (++) ns (00) (++) (00)
Esophagus(150)
Stomach (151)
Small intestine (152)
Colon (153)
Rectum (154)
ns (0+) ns
Gallbladder (155.1)
Pancreas(157)
Peritoneum (158)
Biliary passage/liver (155156 A)
(++)
All sites combined (150— 159) (00) (00)
(+0) (00)
(++) (00)
(00)
(00)
(00)
(0+)
(00)
(00)
(00)
(00)
(00)
(00)
(--) (00)
(00)
Sigurdson
(--)
Levy
Duluth
(0+)
ns
ns
(00) (0+) ns
(+0)
ns
(0+)
ns
ns
ns
(00)
ns
ns
ns
ns
(00)
(00)
(00)
(00)
(00)
(00)
(00)
(00)
(00)
(00)
(++)
(+0) ns
ns
(00)
ns
ns
(+0)
(00) ns
(00)
(00)
(00)
ns
ns
(++)
(0+)
(+ + )
ns
(+0)
(00)
ns
(0+) (00) (00)
ns ns ns ns ns ns
(+0) (00) (00) (00) (++) (0+)
(00)
ns
(00)
(0-)
(00) ns
ns
ns (++) (00)
ns (++)
Tarter Sadler
Utah
ns
(++)
(++)
Conforti
Bay Area, CA Kanarek
ns
Toft
Wigle
Meigs
Quebec
Harrington
Connecticut
Study (site/author)
7
ns
ns
ns
ns
(--) ns
ns
(00)
ns
(00)
Severson
53, 50.
(00)
(00)
(00)
(00)
(00)
(00)
(++)
(00)
(00)
ns
Polissar
Puget Sound, WA
From Marsh, G. M. (1983). Critical review of epidemiologic studies related to ingested asbestos. Environmental Health Perspectives Reproduced by permission. b (Male, female): association with ingested asbestos; + , positive; 0, none; - , negative; ns, not studied.
a
0
Summary of Studies of Gastrointestinal Cancer Risk in Relation to Ingested Asbestos by Cancer Site '*
Gastrointestinal cancer site (ICD 7th revision codes) Mason
Table V
b
a
ns
ns
ns
ns
ns
ns
ns
ns
ns
ns ns
ns
ns ns ns
ns ns ns
(00) (00)
ns
(00)
ns
(00)
(00)
(00)
(00)
ns
ns
ns (+0) ns
ns ns ns
(00) (00)
ns ns
(00) (00)
(+0)
ns ns
ns
(00) (00)
(00)
ns
ns
ns
ns
(00)
ns
ns ns
ns (0+) +
ns
ns ns
(00)
ns
Severson
(+-)
(++)
(+-)
(00)
(00)
+
ns
(00)
(00)
Polissar
Puget Sound, WA
ns
ns
ns
Sadler
Utah
(00)
(00)
(0+)
(00)
(00)
(00)
ns
ns
(0+)
ns
ns
0
ns
(+0)
ns
ns
ns
ns
(+0)
(+0)
ns
Conforti Tarter
Bay Area, CA Kanarek
0
(00)
ns
(00)
Toft
(00)
Wigle
Quebec
0
ns
ns
Harrington Meigs
ns
(00)
ns
Sigurdson
Connecticut
0 ,b
From Marsh, G. M. (1983). Critical review of epidemiologic studies related to ingested asbestos. Environmental Health Perspectives 53, 50. (Male, female): association with ingested asbestos; +, positive; 0, none; - , negative; ns, not studied.
(00)
ns
Bladder (181)
Leukemia, aleukemia (204)
ns
Kidneys (180) (00)
ns
Prostate (177) (males only)
ns
ns
Pleura (162.2)
Brain/CNS (193)
(+0)
Bronchus, trachea, lungs (162, 163)
Thyroid (194)
ns
Buccal cavity and pharynx (140-148)
Levy
Duluth
Study (site/author)
Summary of Studies of Nongastrointestinal Cancer Risk in Relation to Ingested Asbestos by Cancer Site
Nongastrointestinal cancer site (ICD 7th revision codes) Mason
Table VI
39
Asbestos-Contaminated Drinking Water
gastrointestinal sites, esophagus, stomach, perito neum, and pancreas. Epidemiologic studies of the Duluth population, exposed to fibrous amphiboles discharged as taconite tailings, have yet to reveal significant elevations in cancer rates. b. Occupational Studies Epidemiologists have also evaluated gastrointestinal cancer incidence among asbestos workers predi cated on the assumption that a significant proportion of inhaled fibers is trapped in the upper respiratory system, cleared to the throat by the mucociliary escalator, and swallowed. Many of these studies have revealed significantly elevated gastrointestinal cancers in a variety of asbestos-related occupations. A recent meta-analysis that pooled data from pre vious studies (Table VII) found that the incidence of gastrointestinal cancer mortality was significantly correlated with level of exposure. 4. Risk Assessments On the basis of ecological epidemiologic studies, a working group of the Department of Health and Human Services calculated that an exposure to 100 MFL produced an average lifetime risk of 3 3.3 x 10" excess deaths. The Safe Drinking Water Committee of the National Academy of Sciences used gastrointestinal cancer data from occupationally exposed workers to estimate relative risks from drinking asbestos-contaminated water and calcu lated that drinking 0.1 to 0.2 MFL for a 70-year lifespan would cause one excess gastrointestinal cancer death in a population of 100,000. This expo sure estimate was similar to an earlier estimate of 0.5 MFL for the Ambient Water Quality Criteria for Asbestos.
β.
Inhalation
There are mechanisms by which waterborne asbes tos can become airborne and inhalable, a proven pathogenic pathway. Asbestos-contaminated drink ing water can evaporate, leaving asbestos exposed and available for airborne entrainment. In Wood stock, New York, where drinking water was grossly contaminated by deteriorated AC pipes, airborne asbestos levels in affected houses were significantly elevated compared with control houses. However, concentrations did not exceed the range expected in ambient environments. Ultrasonic humidifiers may also generate airborne asbestos from contaminated water. As the tiny water droplets released by these
humidifiers evaporate, tremendously elevated levels of airborne minerals are generated from ordinary tapwater. Fibers in generated droplets may also be come airborne when asbestos-contaminated water is used.
C.
Regulations
In 1991 the U.S. Environmental Protection Agency (EPA) promulgated drinking-water standards that included a Maximum Contaminant Level (MCL) for asbestos of 7 MFL. This MCL was based solely on fibers longer than 10 μ,πι because of a study of labo ratory animals that showed increased intestinal tu mors when exposed to long-fiber asbestos. Public water supply systems that are considered at risk (e.g., AC pipe carrying corrosive water) are required to monitor waterborne concentrations on a nineyear cycle. The EPA in 1989 issued a final rule that will effectively phase out the manufacture of AC pipe by 1996. This rule was not related to health concerns associated with drinking water but rather was part of an overall ban on asbestos use.
/I/. Analysis Traditional analytical chemistry techniques are not capable of detecting asbestos in water because of the ubiquity of its principal elements (Na, Mg, Si, Ca, Fe) in all waters. X-ray diffraction is also poorly suited because of its lack of sensitivity and its inabil ity to distinguish fibrous minerals from their nonfibrous counterparts. Polarized-light microscopy lacks the ability to detect the submicrometer fibers characteristically found in water. Scanning electron microscopy also has resolution limitations and is unable to measure crystalline dimensions, essential for positive asbestos identification. Transmission electron microscopy (TEM) then, is the only method for reliable identification and quantitation of asbes tos in water. TEM is well suited for detecting the very narrow (0.025 μπι) fibers typically found in water, while TEM's electron-diffraction capability, coupled with energy-dispersive x-ray spectroscopy, allows definitive identification of all asbestos species. Water samples are prepared by filtra tion through Ο.Ι-μ,πι-pore polycarbonate filters on which waterborne particles (including asbestos) are trapped. Filter sections are carbon-coated, placed on TEM grids, and the polycarbonate dissolved to leave particles suspended in a carbon film for TEM
Study* (author [year])
Finkelstein [1983, 1984]
Ohlson & Hogstedt [1985]
Gardner [1986]; Gardner and Powell [1986]
Hughes & Weill [1980]; Hughes [1987]
Albin [1983]
1.3
1.4
1.5
1.6
1.7
Selikoff [1979]
McDonald [1980]
3.2
4.3
4.2
4.1
McDonald [1983]. Also Dement [1983]
McDonald [1982]. Also Mancuso and El-Attar [1967]
Enterline & Kendrick [1967]
Amandus & Wheeler [1987] Group 4: Textile workers
3.3
Meurman [1974, 1979]
3.1
Group 3: Miners and millers
2.1
Group 2: Insulators
428 Ontario 107 Ontario
Thomas [1982]
1.2
Plant 2
4,366 Louisiana
2/2.1 (95)
139/77.9 (178)
26/4 (650) 35/11.3 (310)
23/5.7 (404) 8/2.7 (301) High-dose
431/369 (117)
13/14.9 (87) 85/61.1 (139)
2,534 S. Carolina
36/24.4 (148)
31/2.4 (1292) 18/13.9 (129)
39/31.9 (122)
159/147 (108)
Low-dose
104/48.3 (215)
21/5.3 (396)
35/23.6 (148) 14/6.1 (229)
30/8.8 (341)
791/773.1 (102)
20/8.2 (244)
38/28.4 (134) 20/9.0 (223)
11/2.6 (416)
11/7.5 (146)
6/8.1 (74)
.19
186/153.7 (121)
.25
.20
.29
.20
.24
.23
na
.43
161/146.1 (110)
3,291/3,019.3 (109) 213/198.5 (107)
759/688.2 (110)
230/184 (125)
7/2.95 (237)
79/101 (78)
na
1,946/1,376.0 (141)
na
845/277.1 (305)
8/2.4 (333)
397/93.7 (424)
High-dose
54/34.0 (159)
42/47.5 (88)
18/12.7 (142)
177/53.8 (329)
.33
172/157.4 (109) 56/37.8 (148)
19/10.8 (176)
16/6.6 (244)
.26
874/922.7 (95) 226/199.1 (114)
107/74.3 (144)
11/15.0 (73)
15/12.0 (125)
.27
477/522.2 (91)
127/113.9 (112)
48/41.2 (117)
10/8.3 (120)
.25
384/408 (94)
95/97 (98)
35/38 (92)
23/23 (100)
20
.54
20
20
20
20
0
0
20
10
20
10
20
20
0
0
20
15
0
.51
.22
.24
.20
86/47.5 (181) 22/14.7 (150)
261/243.2 (107)
201/213 (94)
All causes
Cancer proportional mortality Latency
220/214 (103)
13/8.5 (153)
44/50.0 (88)
11/9.0 (123)
8/7.5 (107)
11/5.9 (186)
47/44.9 (105)
17/6.5 (264)
7/7.9 (89)
5/5.0 (100)
1/5.9 (17)
9/2.8 (321) 4/0.9 (444)
44/11.6 (379) 12/3.6 (333)
21/4.1 (512) 5/1.2 (413)
48/55.4 (87)
0
Nonmalignant respiratory disease
8/2.8 (285) 1/0.8 (118)
21//22.3 (94)
Lung
All cancer
58/61.0 (95)
AU GI, excl. meso.
28/33.0 (85)
17/11.8 (144)
All Gl, incl. meso.
14/14.1 (99)
ColonGI tract Esophagus Stomach rectum (ICD 150-154)
4,137 Low-dose Pennsylvania
1,843 U.S.
575 Montana
11,379 Quebec
1,092 Finland
17,800 U.S./Canada
1,373 Sweden
Plant 1
Maintenance
Production
Subcohort
2,565 Louisiana
1,510 England
1,176 Sweden
1,592 Wales
Lacquet [1980]
1.1 2,650 Belgium
Number location
Observed/expected counts and SMR for various sites
Summary of Asbestos Workers and Gastrointestinal Cancer Incidence Used in Meta-analysis
Group 1: Cement workers
Cohort No.
Table VII
Peto [1977, 1985]
Puntoni [1977, 1979]
Jones [1980]; Wignall & Fox [1982]
Acheson [1982]
Berry & Newhouse [1983]; Newhouse [1982]
Ohlson [1984]
McDonald [1984]
6.5
6.6
6.7
6.8
6.9 5,969 England
3,641 Connecticut
3,297 Sweden
13,460 England
757 Leyland, UK 570 Blackburn, UK
951 U.K.
2/2.0 (100)
63/23.3 (270)
55/39.9 (138)
1,348 U.S.
Henderson & Enterline [1979]
6.4
7/7.5 (94)
30/51.1 (59)
10/7.6 (132)
59/51.6 (114)
803/740 (109)
37/29.0 (128) 38/29.1 (130)
202/159.7 (127) 109/75.5 (144)
73/49.1 (149) 57/29.1 (196)
333/298.8 (111)
.25
586/727 (81) 144/166 (87)
27/25.7 (105)
.33
.25
.26
.25
1,638/1,689.8 (97)
177/128 (138)
44/41 (109)
6/4.8 (125)
4/3.1 (129)
.30
na
.22
.20
.17
.14
.26
.28
(continues)
0
20
20
10
0
0
0
0
0
0
0
0
0
0
0
.39 .23
0
.32
149/150.8 419/433.1 (97) (99)
219/185 (118)
66/54 (123)
13/6.2 (210)
na
74/66.0 (112)
781/648.7 (120)
173/108.8 (159) 68/39.3 (173)
66/108.8 (61)
567/637.1 (89)
33/21.9 (151)
13/17.4 (75)
98/96.1 (102)
840/943.8 (89)
1,038/1,081.2 (96)
1,073/777.5 (138)
123/67.9 (181) 49/49.4 (99) 1,113/972.9 (114)
45/30.1 (150)
148/69.2 (214)
176/129.7 (136)
24/9.9 (242)
5/4.4 (114)
15/20.9 (72)
4/4.3 (93)
4/3.8 (105)
264 U.S.
Weiss [1977]
6.3
132/134.6 (98)
35/25.9 (124)
36/30.3 (119)
7,510 U.S.
Enterline & Kendrick [1967]
6.2
10/20.3 12/6.3 (49) (190)
46/35.3 (130)
36/40.4 (89)
Enterline & Kendrick 12,402 [1967] U.S.
117/133.0 (88)
265/282.1 (94)
40/15.5 (258) 19/16.3 (116) 260/245.1 (106)
84/119.7 (70)
20/5.6 (361) 4/1.9 (211) 132/100.5 (131)
63/83.3 (76)
6.1
6.10 Acheson [1984]
3/2.1 (145) 4/2.0 (198) 20/26.7 (75)
38/31.0 32/22.2 (144) (123)
4/2.3 (176) 2/1.1 (185) 29/29.0 (100) 304/171.1 (178)
2/5.0 (40)
0/0.5 (0) 0/0.3 (0) 11/6.6 (167) 123/33.9 (362)
4,274 Italy
145 England 283 England 3,211 England
Rossiter & Coles 6,292 England [1980] Group 6: Other industrial workers
5.2
5.1
Group 5: Shipyard workers
4.4
Study* (author [year])
Number location
31,150 England
3,070 Germany 665 Germany
6.13 Hodgson & Jones [1986]
6.14 Woitowitz [1986] Subcohort II
Subcohort I
Post-1969
Pre-1969
Low-dose male High-dose male Low-dose female High-dose female
Subcohort
6/8.8 (68) 0/0.9 (0)
1/2.1 (49)
22/11.9 (185)
5/6.34 (79) 3/1.4 (215
24/24.9 14/27.4 (51) (96) 0/0.2 0/0.3 (0) (0)
9/5.8 (156)
ColonGI tract Esophagus Stomach rectum (ICD 150-154)
All GI, incl. meso. 25/23.3 (107) 42/24.7 (170) 4/2.4 (167) 19/10.8 (176) 11/8.1 (136)
All GI, excl. meso.
197/74.2 (265)
102/20.5 (498)
22/15.3 (144) 9/2.6 (347)
57/50.0 (114) 22/10.3 (213)
152/112.1 na (136) na 1/1.0 (96)
108/72.5 (149) 229/78.7 (291) 12/7.3 (164) 117/36.8 (318) 72/26.5 (272)
All cancer
48/29.7 (162) 110/33.5 (328) 2/0.8 (250) 35/4.2 (833) 38/10.7 (355)
Lung
6/2.6 (231)
50/19.4 (532)
Nonmalignant respiratory disease
Observed/expected counts and SMR for various sites
10 10 10
.30 .50 .46
9 9
.31 .31
10
na 185/194.7 (95) 71/40.7 (175)
10
na
834/931.6 (89) 9/9.5 (95)
5
10
.46
10
.33
.34
Cancer proportional mortality Latency
593/355.9 (167)
319/302.7 (105) 499/310 (161) 40/29.1 (137) 234/126.3 (185) 157/103.4 (152)
All causes
From Frumkin, H., and Berlin, J. (1988). Asbestos exposure and gastrointestinal malignancy review and meta-analysis. American Journal of Industrial Medicine, 14, 79-95. b For complete reference, see original source.
a
933 New Jersey
6.12 Seidman [1986]
1,400 England
6.11 Newhouse & Berry 3,000 [1979]; Newhouse England [1985a]; Newhouse [1973] 700 England
Cohort No.
Table VII (Continued)
43
Asbestos-Contaminated Drinking Water
Woodstock Water - 20,000X
Silicon
Iron
Figure 1 (a) Digitized scanning transmission electron micrograph of asbestos fibers collected in Woodstock, New York, drinking water in 1985. (b-e) X-ray maps depicting relative element concentrations. The crocidolite fiber is distinguished by sodium, silicon, and iron while the chrysotile fiber is distinguished by magnesium and silicon.
Line 1-2 34
Measured r-spacing Pixels 200. 200.
Gold-Ring Diameter (X2.355Ä) 471. 471.
Camera Constant Pixel-A 235.5 235.5
Line 1-2 1-3
Measured Pixels 72.1 64.3
Calculated Angstroms 3.27 3.66
Angle 3-1-2
Measured Degrees 45.5
Reference Degrees 44.7
Reference Angstroms 3.271 3.658
Figure 2 Digitized [212] zone-axis electron diffraction pattern from a crocidolite fiber in the Woodstock sample, (a) Unprocessed CCD-camera pattern with 2.355-Ä gold (internal standard) diffraction ring, (b) Processed pattern with measured r-spacings, calculated d-spacings, and reference i/-spacings.
44
Asbestos-Contaminated Drinking Water
analysis. Figures 1 and 2 illustrate TEM-generated characteristics used in identifying chrysotile and crocidolite asbestos in a drinking-water sample. The current EPA methods, published in 1983, requires analysis of all fibers longer than 0.5 /xm and thus is not fully compatible with the EPA's 1991 MCL, which is based on long (>10 μτη) fibers.
ΙΛ
Control
A variety of technologies is available for removal of asbestos from drinking water. Specific applications will depend on the source of the contamination.
A. Natural
Erosion
When source water is contaminated by asbestos from bedrock, conventional treatments utilizing one or several of the sedimentation, flocculation, co agulation, filtration, or equivalent direct filtra tion methods usually remove 95 to 99% of waterborne asbestos if properly optimized. Dredging of asbestos-laden sediments in rivers or reservoirs may also reduce asbestos concentrations in certain situa tions.
B. Deteriorated
AC Pipes
Deteriorated AC pipes often contribute asbestos contamination on a localized level. In several epi sodes, complaints about fibers clogging faucet strainers were the first hints of AC-deterioration problems. Deterioration and resultant contaminant problems may not always be detectable using TEM analysis and the EPA's MCL because of the spo
radic nature of the problem and the fact that more than 95% of waterborne asbestos fibers are usually shorter than 10 μηι. For example, tap water in Woodstock, New York, which had a visible fiber suspension and contained more than 1000 MFL (based on all fiber sizes), was below the ΙΟ-μπιlength-based MCL of 7 MFL. TEM analysis for all fiber sizes and a visual inspection of AC pipes should be part of routine monitoring. In instances where deterioration is caused by cor rosive water, chemical treatments may be applied to reduce the corrosivity. Lime treatment applied in a consistent manner is often effective in reducing acidity, a common promoter of AC-pipe deteriora tion. Chemicals may also be added to form a protec tive lining inside the pipe; zinc salts have proven effective in some cases. Pipes may also be physi cally cleaned and lined with asphalt or rubberized compounds to minimize deterioration. Future con tamination problems can be minimized by following recommended practices when installing or modify ing AC pipe. Finally, AC pipes may be bypassed or replaced by non-AC pipes.
Bibliography Frumkin, H., and Berlin, J. (1988). Asbestos exposure and gas trointestinal malignancy: Review and meta-analysis. Ameri can Journal of Industrial Medicine, 14, 79-95. Schreier, Η. (1989). "Studies in Environmental Science 37: As bestos in the Natural Environment." Elsevier, Amsterdam. Summary workshop on ingested asbestos, (1983). Environmental Health Perspectives, 53, 1-204. Toft, P., Meek, Μ. E., Wigle, D. T., and Meranger, J. C. (1984). Asbestos in drinking water. CRC Critical Reviews in Environ mental Control, 14(2), 151-197. Webber, J. S., and Covey, J. R. (1991). Asbestos in water. CRC Critical Reviews in Environmental Control, 21(4), 331-371.
I. II. III. IV. V.
Mineralogy and History Occurrence Health Hazards Analysis Control
Glossary Asbestosis Nonmalignant, dose-related, lung dis ease (pneumoconiosis) marked by interstitial fi brosis and reduced pulmonary efficiency. Aspect ratio Fiber length divided by fiber width. Mesothelioma Rare malignant tumor of the body linings (pleura, peritoneum, or pericardium) which grows diffusely as a thick sheet covering the viscera. Micrometer (μιη) One thousandth of a millimeter. + pH Negative logarithm (base 10) of the H con centration in water. Water with pH <7 is con sidered acidic and water with pH > 7 is considered alkaline. Standardized mortality ratio (SMR) Ratio of mor tality in a study group divided by the expected mortality from a control group. The ratio is usu ally expressed as percentile, with values less than 100 indicating lowered mortality among the study group and values greater than 100 indicating higher mortality among the study group. Transmigration Ability of particles to pass from the digestive tract through the intestinal wall and into the circulatory system.
ASBESTOS is α collective term that describes natu rally occurring hydrated silicate minerals that break into fibers. Asbestos is naturally present in some water bodies but its accelerated use in the twentieth
century has increased its concentration in many other water systems. Although ingested asbestos does not appear to be as hazardous as airborne asbestos, some ingested asbestos undoubtedly reaches the bloodstream and a few studies have revealed a possible link between this migration and tumors at areas remote from the pulmonary or di gestive systems. Some epidemiologic studies of pop ulations drinking asbestos-contaminated water have detected increased gastrointestinal cancer. A prudent course of action is to minimize asbestoscontamination in drinking water through proven, cost-effective methods.
I. Mineralogy
and History
A. Semantics, Mineralogy, and Properties The ancient Greeks called these flexible, fireresistant minerals ctaßsaros, meaning inextin guishable or unquenchable. Asbestos characteris tically breaks into very thin fibers, often as narrow as 0.025 μιη in diameter, which have high resistance to heat and have enormous tensile strength. Defini tions for asbestos have changed over the centuries as new varieties have been identified and as classifi cation systems have evolved. Controversy over pre cise definitions continue today because of differ ences in regulatory and commercial perspectives. Six mineral types are currently recognized as as bestos (Table I). The sole serpentine variety, chrysotile, is the most common type of asbestos, ac counting for more than 90% of worldwide production. Chrysotile is the most flexible of the asbestos types and is the most vulnerable to leaching by acids. Its structure is unique among asbestos varieties—a magnesium hydroxide layer overlies a
Handbook of Hazardous Materials Copyright © 1993 by Academic Press, Inc. All rights of reproduction in any form reserved.
23
30
Asbestos-Contaminated Drinking Water
Table I Characteristics of Asbestos Minerals Mineral type
Variety
Chemical formula
Serpentine
Chrysotile
Mg 3(Si 20 5)(OH) 4
Amphibole
Amosite (grunerite)
(Fe,Mg) 7(Si 80 2 2)(OH) 2
Crocidolite (riebeckite)
Na 2Fe 5(Si 80 2 2)(OH) 2
Anthophyllite
(Mg,Fe) 7(Si 80 2 2)(OH) 2
Tremolite
Ca 2Mg 5(Si 80 2 2)(OH) 2
Actinolite
Ca 2(Mg,Fe) 5(Si 80 2 2)(OH) 2
silicate layer, forming an elongated scroll. The five amphibole asbestos types have more typical struc ture, with double-chain silicates sandwiching a cation (Fe, Mg, Na, or Ca) layer. Crocidolite is an iron- and sodium-rich riebeckite asbestos that has higher tensile strength than any other asbestos type. Amosite, an iron- and magnesium-rich grunerite fi ber, is highly resistant to leaching. Anthophyllite is a magnesium-rich amphibole that has the highest fu sion point. Tremolite and actinolite are in a calciumiron replacement series and are of little commercial significance.
0. History of Asbestos and Humans Although asbestos was woven into fireproof cloth by ancient Greeks and used as lamp wicks in medieval times, its utilization was fairly limited until the be ginning of the twentieth century. At about that time, people began to recognize the diverse technological applications of the unique properties of asbestos, namely its thermal and electrical resistance, tremen dous tensile strength, chemical resistance, flexibil ity, and low cost. In response to escalating de mands, asbestos production increased more than 100-fold during the first eight decades of the cen tury. Thousands of uses have been described for asbestos, ranging from sprayed-on fireproofing and insulation to brake linings, floor tiles, shingles, asbestos-cement pipes, and missile covers. An increase in disease was inevitable as the ex ploitation of asbestos accelerated during the twentieth century. In some instances, however, these elevations were not noted immediately be cause of the latency period, usually measured in decades, between the time of exposure and the man ifestation of symptoms. Asbestosis was first docu
mented around 1930 in asbestos workers and shortly thereafter, increased incidences of lung cancer were also noted. Following World War II, an alarming increase in mesothelioma, a previously rare disease, was noted not only in asbestos workers but also in persons marginally exposed to asbestos. Because these diseases were associated with inhalation of airborne asbestos fibers, increasingly stringent regu lations have been enacted during the past few de cades to reduce exposure of workers and the public to airborne fibers. Does asbestos-contaminated drinking water pose a health hazard similar to airborne asbestos? Most studies have indicated that, while there may be some health risks associated with ingestion of asbestos, the health hazards are substantially less than those posed by inhalation. This is discussed in more detail in Section III.
Occurrence
II.
A. Large-Scale
Surveys
The majority of water-supply systems in North America contain less than one million asbestos fi bers per liter (MFL). A survey of several hundred systems in the United States revealed that more than 80% had less than one MFL while only 10% had more than ten MFL (Table II). Similarly, in Canada 5% of the population receive more than one MFL while less than 1% receive more than 100 MFL. Comparable surveys in Europe have revealed simi lar patterns. Table II Distribution of Reported Asbestos Concentrations in Drinking Water from 406 Cities in 47 0 States, Puerto Rico, and the District of Columbia Highest asbestos concentration 6 (10 fibers/L)
Number of cities
Percentage
Below detectable limits
117
28.8
<1
216
53.2
1-10
33
8.1
>10
40
9.9
Total
406
100
" From Millette, J. R., Clark, P. J., Stober, J., and Rosenthal, M. (1983). Asbestos in water supplies of the United States. Envi ronmental Health Perspectives, 53, 45. Reproduced by per mission.
31
Asbestos-Contaminated Drinking Water
B. Episodes of Gross
Contamination
In spite of the generally low asbestos concentrations in public water-supply systems, there have been several instances where concentrations have been drastically elevated. While some of the highest con centrations were from non-point sources, pointsource contamination was also significant on a local ized level. 1 . Natural Erosion Some of the highest waterborne concentrations of asbestos have been measured in areas of serpentinized bedrock where erosional processes often en train chrysotile into drinking water. In eastern North America, such outcroppings have produced concen trations of more than 1000 MFL in Quebec and New foundland. Likewise, erosion of serpentinized de posits in California have generated concentrations in excess of 10,000 MFL. Further north in Washing ton State, chrysotile concentrations have exceeded 100 MFL due to erosion. Chrysotile fibers produced by natural erosion are generally small, usually less than 1 μιη in length. Elevated amphibole asbestos concentrations are rarely encountered in natural wa ters of North America. 2. Deteriorated AC Pipe Asbestos fibers are susceptible to sloughing off the inner surfaces of deteriorated AC pipes during trans mission of water. Corrosive water often accelerates this process by dissolving the cement matrix of the AC pipe. An Aggressiveness Index (A.I.) has been proposed by the American Water Works Associa
Table III
tion to predict the potential for water to corrode AC pipe. This is defined as A.I. = pH + log 1 0 [alkalinity (mg/L as CaC0 3 ) + hardness (mg/L as C a C 0 3 ) ] . Indices less than 10 are considered highly aggres sive. In a South Carolina drinking water system, corrosive water's disintegration of AC pipe was blamed for chrysotile concentrations in excess of 500 MFL. In Woodstock, New York, concentra tions of chrysotile and crocidolite in excess of 1000 MFL were attributed to long-term degradation of AC pipe by acidic water. Factors such as seasonal use, drastic changes in water pressure, and improper tapping and cutting operations can also contribute to elevated concentrations.
3. Anthropogenic Disturbances One of the most widely reported contamination epi sodes was discovered in Duluth, Minnesota during the 1970s. An iron-mining operation had been dis posing of taconite tailing wastes into western Lake Superior for two decades; amphibole fibers from these tailings eventually turned up in the unfiltered drinking water of Duluth. During times of turbu lence, concentrations would reach 600 MFL. This dumping was eventually stopped and Duluth insti tuted filtration to remove residual fibers from the drinking water. In another instance, concentrations of up to 74 MFL were blamed on an old asbestos waste pile in Kentucky.
Some Size Characteristics of Asbestos Fibers Found in Various Water Supplies
Source
Type of fiber
0
Number of fibers measured
Average length (μηι)
Average width (μτη)
Average aspect ratio
Maximum length found (μτη)
Reservoir with natural erosion (WA)
Chrysotile
289
0.8
0.034
25:1
3
Reservoir with natural erosion (CA)
Chrysotile
644
1.3
0.04
39: 1
10
Cistern with asbestos tile roof (VI)
Chrysotile
342
2.3
0.04
62: 1
25
Distribution sites from five asbestos cement pipe systems (SC, PA, FL)
Chrysotile
1440
4.3
0.044
121 : 1
80
Lake Superior (MN)
Amphibole
468
1.5
0.18
11: 1
14
α
From Millette, J. R., Clark, P. J., Pansing, M. F., and Twyman, J. D. (1980). Concentration and size of asbestos in water supplies. Environmental Health Perspectives 34, 22, Reproduced by permission.
Asbestos-Contaminated Drinking Water
32
C. Characteristics of Waterborne Asbestos As previously discussed, chrysotile is the dominant asbestos type identified in water samples. This re flects its widespread use in industry and its abun dance in nature. Chrysotile, with its unique positive surface charge, is vulnerable to attack by acids and may degrade in low-pH water systems. Amphiboles, on the other hand, are more impervious to disso lution but are rarely encountered in drinking wa ter samples. Amphiboles are often minor cocontaminants with chrysotile when deteriorated AC pipes are the asbestos source. Asbestos-like mineral fibers such as halloysite, rutile, and palygorskite have been occasionally detected in water systems but little is known about potential biological effects of ingestion of these fiber types. Asbestos fibers resulting from AC pipe or anthro pogenic activity usually have larger dimensions than fibers from natural erosion sources (Table III). Indi vidual fiber length, width, and especially mass 2 (length x width x density) are often distinctly larger from human-derived sources.
III. Health
Hazards
Although evidence that inhalation of asbestos can cause serious health problems is overwhelming, health risks posed by ingestion of asbestos are ap parently much lower.
A.
of the intestines. One drawback in relating these feed studies to ingestion of waterborne asbestos is that most animal studies were performed with much longer fibers than are normally found in asbestoscontaminated drinking water. In addition, asbestos fibers embedded in food pellets used in the animal studies may behave differently from the loose fibers characteristic in drinking water. 2. Transmigration Studies Asbestos fibers typically found in contaminated drinking water are small enough to pass through the wall of the small intestine and into the blood and lymph fluid. Most studies that have investigated this possibility have found that fibers do indeed reach the 7 circulatory system, probably at a ratio of ΙΟ" to 3 10~ of the fiber concentrations ingested. Elevated concentrations of amphibole fibers were measured in the urine of Duluth residents who had been drink ing contaminated Lake Superior water. Several studies on asbestos workers have also detected in creased asbestos levels in urine. Elevated asbestos concentrations have been detected in various tissues and organs of laboratory animals that have ingested asbestos. Many of these human and animal studies have found a preferential transmigration of small fibers (usually shorter than 2 μ,πι), the size range most common to drinking water. Some case studies of cancers of digestive and urinary organs in asbes tos workers have revealed asbestos fibers in these organs. However, a larger body of evidence with controls will have to be accumulated before defini tive linkages can be established.
Ingestion
1 . Animal Toxicity Studies Most investigations of asbestos ingestion by labora tory animals have failed to produce evidence of tox icity or consistent, reproducible, organ-specific car cinogenicity. The largest series of studies was performed by the National Toxicology Program (NTP), under the auspices of the National Institute for Environmental Health Sciences, in which large numbers of diverse rodent populations were fed a variety of asbestos types. With the exception of one study that revealed an increase in large-intestine tu mors, all other NTP studies revealed no significant health differences between experimental and con trol populations. While most other studies have sim ilarly failed to demonstrate pathogenicity of ingested asbestos (Table IV), there have been indications of induced abnormalities such as impeded permeability
3. Epidemiologic Studies a. Ecological Studies More than a dozen epidemiologic studies investi gated possible correlations between asbestoscontaminated drinking water and cancer mortality. Certain investigations have revealed statistically significant correlations with various organs and tis sues, but most have not revealed a definitive associ ation (Tables V and VI). Some of the most signifi cant studies have focused on the San Francisco Bay area, where long-term contamination of water by chrysotile has resulted from natural erosion of serpentinized bedrock. A large population and population-based cancer registries in the Bay Area have increased statistical sensitivity and enhanced meaningful analyses. Several investigations there have revealed positive correlations for combined
Species Rat
Rat
Rat
Rat
Bonser [1967]
Gross [1974]
Gibel [1976]
Cunningham [1977] 1% in diet ad libitum
0 1% in diet ad libitum
Control Chrysotile
0
Control Chrysotile
20 mg/day
Talc
0
Control 20 mg/day
10 mg/wk
Crocidolite (2 sources) Chrysotile
10 mg/wk
5 mg/wk
Crocidolite 0
10 mg/wk
Chrysotile
Control
0
Control
Crocidolite
5% in diet ad libitum
0
Control Chrysotile
0.15% in diet ad libitum
Dose
0
Crocidolite
Test material
Summary of Asbestos Ingestion Studies
Study (author [date])
Table IV
To 24 mo
0
To 24 mo
0
Life
Life
0
18 wk
0
16 wk
16 wk
16 wk
0
21 mo
0
To 78 wk
Exposure time
c
£
To 30 mo
6 24 mo
To 24 mo
702
649
441
c
To 1.5 yr
To 1.5 yr
To 1.5 yr
To 1.5 yr
To 1.5 yr
To 1.5 yr
21 mo
21 mo
To 86 wk
To 78 wk
Study duration
•0/36
'J/8
10/7
50/49
50/45
50/42
24/24
63/63
24/24
34/34
33/33
31/31
5/5
10/10
65/25
40/12
Number of animals (initial/ examined)
11
1
6
2
3
12
0
0
5
1
0
2
0
0
1
0
Number
2 Thyroid Thyroid Liver Chemodectoma jugular body
Peritoneum
Brain Pituitary Node 2 Kidney Peritoneum
Liver
Liver
Lung 4 Kidney 3 Node 4 Liver
3 Breast Thigh Node
Node
Breast
Liver
Location
c
C S
S
S C L C S
C
C
C C L C
C S L
L
C
S
Type*
(continues)
Malignant tumors
Species
Rat
Hamster
Rat
Study (author [date])
Wagner [1977]
Smith [1980]
Bonham [1980]
Table IV (Continued)
0
Control
Control
Cellulose fiber
Chrysotile
Control
Taconite tailings
Taconite tailings
Taconite tailings
Amosite
Amosite
libitum
0
ad
libitum
10% in diet
ad
10% in diet
0
libitum
50 mg/L ad
libitum
5 mg/L ad
libitum
0.5 mg/L ad
libitum
50 mg/L ad
libitum
5 mg/L ad
libitum
0.5 mg/L ad
100 mg/day
Talc
Amosite
100 mg/day
0
Dose
Chrysotile
Control
Test material
0
To 32 mo
To 32 mo
0
To 23 mo
To 23 mo
To 23 mo
To 23 mo
To 23 mo
To 23 mo
0
101 days/5 mo
101 days/5 mo
0
Exposure time
£
c
c
To 32 mo
To 32 mo
To 32 mo
To 23 mo
To 23 mo
To 23 mo
To 23 mo
To 23 mo
To 23 mo
To 23 mo
641
614
619
To 30 mo
121/115
242/197
240/189
120/120
60/60
60/60
60/60
60/60
60/60
60/60
16/16
32/32
32/32
40/32
Number of animals (initial/ Study duration examined)
3
2
4
1
0
0
1
0
3
1
0
3
3
11
Number
Colon
Colon
3 Colon Abdominal mesothelioma
Node
Uterus
2 Stomach Peritoneal mesothelioma
Lung
2 Uterus Stomach
Node Stomach Uterus
Thyroid Liver 2 Adrenal Kidney Node 5 Fat
Colon Ileum Adrenal 2 Node Bone
Location
Malignant tumors
C
c
C
L
S
C
C
S S
L S S
L S
c c c c
L S
s c
C
Type*
Rat
Rat
Rat
Ward [1980]
Ward [1980]
Hiding [1981]
100 MFL ad libitum
5,000 MFL ad libitum
100,000 MFL ad libitum
Unfiltered Duluth tapwater
Lake Superior water sediment
Taconite tailings
l/wk(SC) 10 mg 3/wk
Saline plus amosite 1 MFL ad libitum
7.4 mg/kg wk 10 mg 3/wk
Azoxymethane plus amosite
Filtered Duluth tapwater
7.4 mg/kg wk
Azoxymethane
—
1.0 mL 3/wk (gavage)
Saline Untreated
10 mg 3/wk 10 mg 3/wk
7.4 mg/kg wk 10 mg 3/wk
Azoxymethane plus chrysotile
Chrysotile
7.4 mg/kg wk 10 mg 3/wk
Azoxymethane plus amosite
Amosite
7.4 mg/kg wk
Azoxymethane'*
870
840
c
c
c
c
960
690
10 wk
10 wk
10 wk
0
10 wk
10 wk
10 wk
10 wk
10 wk
10 wk
870
c
c
c
£
840
960
690
To95wk
To95wk
To95wk
34 wk
34 wk
34 wk
34 wk
34 wk
34 wk
34 wk
30/30
22/22
30/28
28/27
50/49
50/48
50/48
21/21
21/21
21/21
21/21
21/21
21/18
21/21
3
3
4
3
17
44
39
0
0
0
0
10
10
12
Neck Chest wall Mediastinum
Lung Skin Uterus
Salivary gland Skin Uterus Mediastinum
Lung Ovary Forestomach
Ileum 16 Colon
15 Ileum 29 Colon
12 Ileum 27 Colon
4 Ileum 6 Colon
5 Ileum 7 Colon 3 Ileum 7 Colon
(continues)
S S L
C C S
C C S L
C C C
C C
C C
C C
C C
C C C C
Rat
Bolton [1982]
Life Life
840
25 mo. 25 mo. 25 mo.
250 mg/wk 250 mg/wk 250 mg/wk
0
0
Amosite Crocidolite Chrysotile
Margarine control
Control
Fat Pleural histiocytoma 2 Adrenal Plasma cell tumor 2 Adrenal Bladder Peritoneum Fat Lymphoma
1 5
4
2
22/22
24/24
23/23
Life
Life
Life
0
0
Stomach Adrenal
1 22/22
Salivary gland 2 Uterus Skin Peritoneal mesothelioma
Leukemia
Breast 2 Fibrous histiocytoma Skin Mediastinum Pleural mesothelioma
24/24
1
6
Location
5
20/20
30/30
Number
Malignant tumors
30/30
840
£
£
20 mg/day
750
Diatomaceous earth
c
c
750
300 mg/day
£
Amosite
870
870
£
Study duration
20 mg/day
Dose
Exposure time
Chrysotile/amosite
Test material
Number of animals (initial/ examined)
s
c c s
c
c s s
S
C S C
C L
C
Type*
From Condie, L. W. (1983). Review of published studies of orally administered asbestos. Environmental Health Perspectives 53,4-7. Reproduced by permission. * Type C, carcinoma; S, sarcoma, L, lymphoma. £ Mean survival time in days. d Azoxymethane given subcutaneously; saline administered by oral gavage or subcutaneously.
a
Species
(Continued)
Study (author [date])
Table IV
(+-) (++) ns (00) (++) (00)
Esophagus(150)
Stomach (151)
Small intestine (152)
Colon (153)
Rectum (154)
ns (0+) ns
Gallbladder (155.1)
Pancreas(157)
Peritoneum (158)
Biliary passage/liver (155156 A)
(++)
All sites combined (150— 159) (00) (00)
(+0) (00)
(++) (00)
(00)
(00)
(00)
(0+)
(00)
(00)
(00)
(00)
(00)
(00)
(--) (00)
(00)
Sigurdson
(--)
Levy
Duluth
(0+)
ns
ns
(00) (0+) ns
(+0)
ns
(0+)
ns
ns
ns
(00)
ns
ns
ns
ns
(00)
(00)
(00)
(00)
(00)
(00)
(00)
(00)
(00)
(00)
(++)
(+0) ns
ns
(00)
ns
ns
(+0)
(00) ns
(00)
(00)
(00)
ns
ns
(++)
(0+)
(+ + )
ns
(+0)
(00)
ns
(0+) (00) (00)
ns ns ns ns ns ns
(+0) (00) (00) (00) (++) (0+)
(00)
ns
(00)
(0-)
(00) ns
ns
ns (++) (00)
ns (++)
Tarter Sadler
Utah
ns
(++)
(++)
Conforti
Bay Area, CA Kanarek
ns
Toft
Wigle
Meigs
Quebec
Harrington
Connecticut
Study (site/author)
7
ns
ns
ns
ns
(--) ns
ns
(00)
ns
(00)
Severson
53, 50.
(00)
(00)
(00)
(00)
(00)
(00)
(++)
(00)
(00)
ns
Polissar
Puget Sound, WA
From Marsh, G. M. (1983). Critical review of epidemiologic studies related to ingested asbestos. Environmental Health Perspectives Reproduced by permission. b (Male, female): association with ingested asbestos; + , positive; 0, none; - , negative; ns, not studied.
a
0
Summary of Studies of Gastrointestinal Cancer Risk in Relation to Ingested Asbestos by Cancer Site '*
Gastrointestinal cancer site (ICD 7th revision codes) Mason
Table V
b
a
ns
ns
ns
ns
ns
ns
ns
ns
ns
ns ns
ns
ns ns ns
ns ns ns
(00) (00)
ns
(00)
ns
(00)
(00)
(00)
(00)
ns
ns
ns (+0) ns
ns ns ns
(00) (00)
ns ns
(00) (00)
(+0)
ns ns
ns
(00) (00)
(00)
ns
ns
ns
ns
(00)
ns
ns ns
ns (0+) +
ns
ns ns
(00)
ns
Severson
(+-)
(++)
(+-)
(00)
(00)
+
ns
(00)
(00)
Polissar
Puget Sound, WA
ns
ns
ns
Sadler
Utah
(00)
(00)
(0+)
(00)
(00)
(00)
ns
ns
(0+)
ns
ns
0
ns
(+0)
ns
ns
ns
ns
(+0)
(+0)
ns
Conforti Tarter
Bay Area, CA Kanarek
0
(00)
ns
(00)
Toft
(00)
Wigle
Quebec
0
ns
ns
Harrington Meigs
ns
(00)
ns
Sigurdson
Connecticut
0 ,b
From Marsh, G. M. (1983). Critical review of epidemiologic studies related to ingested asbestos. Environmental Health Perspectives 53, 50. (Male, female): association with ingested asbestos; +, positive; 0, none; - , negative; ns, not studied.
(00)
ns
Bladder (181)
Leukemia, aleukemia (204)
ns
Kidneys (180) (00)
ns
Prostate (177) (males only)
ns
ns
Pleura (162.2)
Brain/CNS (193)
(+0)
Bronchus, trachea, lungs (162, 163)
Thyroid (194)
ns
Buccal cavity and pharynx (140-148)
Levy
Duluth
Study (site/author)
Summary of Studies of Nongastrointestinal Cancer Risk in Relation to Ingested Asbestos by Cancer Site
Nongastrointestinal cancer site (ICD 7th revision codes) Mason
Table VI
39
Asbestos-Contaminated Drinking Water
gastrointestinal sites, esophagus, stomach, perito neum, and pancreas. Epidemiologic studies of the Duluth population, exposed to fibrous amphiboles discharged as taconite tailings, have yet to reveal significant elevations in cancer rates. b. Occupational Studies Epidemiologists have also evaluated gastrointestinal cancer incidence among asbestos workers predi cated on the assumption that a significant proportion of inhaled fibers is trapped in the upper respiratory system, cleared to the throat by the mucociliary escalator, and swallowed. Many of these studies have revealed significantly elevated gastrointestinal cancers in a variety of asbestos-related occupations. A recent meta-analysis that pooled data from pre vious studies (Table VII) found that the incidence of gastrointestinal cancer mortality was significantly correlated with level of exposure. 4. Risk Assessments On the basis of ecological epidemiologic studies, a working group of the Department of Health and Human Services calculated that an exposure to 100 MFL produced an average lifetime risk of 3 3.3 x 10" excess deaths. The Safe Drinking Water Committee of the National Academy of Sciences used gastrointestinal cancer data from occupationally exposed workers to estimate relative risks from drinking asbestos-contaminated water and calcu lated that drinking 0.1 to 0.2 MFL for a 70-year lifespan would cause one excess gastrointestinal cancer death in a population of 100,000. This expo sure estimate was similar to an earlier estimate of 0.5 MFL for the Ambient Water Quality Criteria for Asbestos.
β.
Inhalation
There are mechanisms by which waterborne asbes tos can become airborne and inhalable, a proven pathogenic pathway. Asbestos-contaminated drink ing water can evaporate, leaving asbestos exposed and available for airborne entrainment. In Wood stock, New York, where drinking water was grossly contaminated by deteriorated AC pipes, airborne asbestos levels in affected houses were significantly elevated compared with control houses. However, concentrations did not exceed the range expected in ambient environments. Ultrasonic humidifiers may also generate airborne asbestos from contaminated water. As the tiny water droplets released by these
humidifiers evaporate, tremendously elevated levels of airborne minerals are generated from ordinary tapwater. Fibers in generated droplets may also be come airborne when asbestos-contaminated water is used.
C.
Regulations
In 1991 the U.S. Environmental Protection Agency (EPA) promulgated drinking-water standards that included a Maximum Contaminant Level (MCL) for asbestos of 7 MFL. This MCL was based solely on fibers longer than 10 μ,πι because of a study of labo ratory animals that showed increased intestinal tu mors when exposed to long-fiber asbestos. Public water supply systems that are considered at risk (e.g., AC pipe carrying corrosive water) are required to monitor waterborne concentrations on a nineyear cycle. The EPA in 1989 issued a final rule that will effectively phase out the manufacture of AC pipe by 1996. This rule was not related to health concerns associated with drinking water but rather was part of an overall ban on asbestos use.
/I/. Analysis Traditional analytical chemistry techniques are not capable of detecting asbestos in water because of the ubiquity of its principal elements (Na, Mg, Si, Ca, Fe) in all waters. X-ray diffraction is also poorly suited because of its lack of sensitivity and its inabil ity to distinguish fibrous minerals from their nonfibrous counterparts. Polarized-light microscopy lacks the ability to detect the submicrometer fibers characteristically found in water. Scanning electron microscopy also has resolution limitations and is unable to measure crystalline dimensions, essential for positive asbestos identification. Transmission electron microscopy (TEM) then, is the only method for reliable identification and quantitation of asbes tos in water. TEM is well suited for detecting the very narrow (0.025 μπι) fibers typically found in water, while TEM's electron-diffraction capability, coupled with energy-dispersive x-ray spectroscopy, allows definitive identification of all asbestos species. Water samples are prepared by filtra tion through Ο.Ι-μ,πι-pore polycarbonate filters on which waterborne particles (including asbestos) are trapped. Filter sections are carbon-coated, placed on TEM grids, and the polycarbonate dissolved to leave particles suspended in a carbon film for TEM
Study* (author [year])
Finkelstein [1983, 1984]
Ohlson & Hogstedt [1985]
Gardner [1986]; Gardner and Powell [1986]
Hughes & Weill [1980]; Hughes [1987]
Albin [1983]
1.3
1.4
1.5
1.6
1.7
Selikoff [1979]
McDonald [1980]
3.2
4.3
4.2
4.1
McDonald [1983]. Also Dement [1983]
McDonald [1982]. Also Mancuso and El-Attar [1967]
Enterline & Kendrick [1967]
Amandus & Wheeler [1987] Group 4: Textile workers
3.3
Meurman [1974, 1979]
3.1
Group 3: Miners and millers
2.1
Group 2: Insulators
428 Ontario 107 Ontario
Thomas [1982]
1.2
Plant 2
4,366 Louisiana
2/2.1 (95)
139/77.9 (178)
26/4 (650) 35/11.3 (310)
23/5.7 (404) 8/2.7 (301) High-dose
431/369 (117)
13/14.9 (87) 85/61.1 (139)
2,534 S. Carolina
36/24.4 (148)
31/2.4 (1292) 18/13.9 (129)
39/31.9 (122)
159/147 (108)
Low-dose
104/48.3 (215)
21/5.3 (396)
35/23.6 (148) 14/6.1 (229)
30/8.8 (341)
791/773.1 (102)
20/8.2 (244)
38/28.4 (134) 20/9.0 (223)
11/2.6 (416)
11/7.5 (146)
6/8.1 (74)
.19
186/153.7 (121)
.25
.20
.29
.20
.24
.23
na
.43
161/146.1 (110)
3,291/3,019.3 (109) 213/198.5 (107)
759/688.2 (110)
230/184 (125)
7/2.95 (237)
79/101 (78)
na
1,946/1,376.0 (141)
na
845/277.1 (305)
8/2.4 (333)
397/93.7 (424)
High-dose
54/34.0 (159)
42/47.5 (88)
18/12.7 (142)
177/53.8 (329)
.33
172/157.4 (109) 56/37.8 (148)
19/10.8 (176)
16/6.6 (244)
.26
874/922.7 (95) 226/199.1 (114)
107/74.3 (144)
11/15.0 (73)
15/12.0 (125)
.27
477/522.2 (91)
127/113.9 (112)
48/41.2 (117)
10/8.3 (120)
.25
384/408 (94)
95/97 (98)
35/38 (92)
23/23 (100)
20
.54
20
20
20
20
0
0
20
10
20
10
20
20
0
0
20
15
0
.51
.22
.24
.20
86/47.5 (181) 22/14.7 (150)
261/243.2 (107)
201/213 (94)
All causes
Cancer proportional mortality Latency
220/214 (103)
13/8.5 (153)
44/50.0 (88)
11/9.0 (123)
8/7.5 (107)
11/5.9 (186)
47/44.9 (105)
17/6.5 (264)
7/7.9 (89)
5/5.0 (100)
1/5.9 (17)
9/2.8 (321) 4/0.9 (444)
44/11.6 (379) 12/3.6 (333)
21/4.1 (512) 5/1.2 (413)
48/55.4 (87)
0
Nonmalignant respiratory disease
8/2.8 (285) 1/0.8 (118)
21//22.3 (94)
Lung
All cancer
58/61.0 (95)
AU GI, excl. meso.
28/33.0 (85)
17/11.8 (144)
All Gl, incl. meso.
14/14.1 (99)
ColonGI tract Esophagus Stomach rectum (ICD 150-154)
4,137 Low-dose Pennsylvania
1,843 U.S.
575 Montana
11,379 Quebec
1,092 Finland
17,800 U.S./Canada
1,373 Sweden
Plant 1
Maintenance
Production
Subcohort
2,565 Louisiana
1,510 England
1,176 Sweden
1,592 Wales
Lacquet [1980]
1.1 2,650 Belgium
Number location
Observed/expected counts and SMR for various sites
Summary of Asbestos Workers and Gastrointestinal Cancer Incidence Used in Meta-analysis
Group 1: Cement workers
Cohort No.
Table VII
Peto [1977, 1985]
Puntoni [1977, 1979]
Jones [1980]; Wignall & Fox [1982]
Acheson [1982]
Berry & Newhouse [1983]; Newhouse [1982]
Ohlson [1984]
McDonald [1984]
6.5
6.6
6.7
6.8
6.9 5,969 England
3,641 Connecticut
3,297 Sweden
13,460 England
757 Leyland, UK 570 Blackburn, UK
951 U.K.
2/2.0 (100)
63/23.3 (270)
55/39.9 (138)
1,348 U.S.
Henderson & Enterline [1979]
6.4
7/7.5 (94)
30/51.1 (59)
10/7.6 (132)
59/51.6 (114)
803/740 (109)
37/29.0 (128) 38/29.1 (130)
202/159.7 (127) 109/75.5 (144)
73/49.1 (149) 57/29.1 (196)
333/298.8 (111)
.25
586/727 (81) 144/166 (87)
27/25.7 (105)
.33
.25
.26
.25
1,638/1,689.8 (97)
177/128 (138)
44/41 (109)
6/4.8 (125)
4/3.1 (129)
.30
na
.22
.20
.17
.14
.26
.28
(continues)
0
20
20
10
0
0
0
0
0
0
0
0
0
0
0
.39 .23
0
.32
149/150.8 419/433.1 (97) (99)
219/185 (118)
66/54 (123)
13/6.2 (210)
na
74/66.0 (112)
781/648.7 (120)
173/108.8 (159) 68/39.3 (173)
66/108.8 (61)
567/637.1 (89)
33/21.9 (151)
13/17.4 (75)
98/96.1 (102)
840/943.8 (89)
1,038/1,081.2 (96)
1,073/777.5 (138)
123/67.9 (181) 49/49.4 (99) 1,113/972.9 (114)
45/30.1 (150)
148/69.2 (214)
176/129.7 (136)
24/9.9 (242)
5/4.4 (114)
15/20.9 (72)
4/4.3 (93)
4/3.8 (105)
264 U.S.
Weiss [1977]
6.3
132/134.6 (98)
35/25.9 (124)
36/30.3 (119)
7,510 U.S.
Enterline & Kendrick [1967]
6.2
10/20.3 12/6.3 (49) (190)
46/35.3 (130)
36/40.4 (89)
Enterline & Kendrick 12,402 [1967] U.S.
117/133.0 (88)
265/282.1 (94)
40/15.5 (258) 19/16.3 (116) 260/245.1 (106)
84/119.7 (70)
20/5.6 (361) 4/1.9 (211) 132/100.5 (131)
63/83.3 (76)
6.1
6.10 Acheson [1984]
3/2.1 (145) 4/2.0 (198) 20/26.7 (75)
38/31.0 32/22.2 (144) (123)
4/2.3 (176) 2/1.1 (185) 29/29.0 (100) 304/171.1 (178)
2/5.0 (40)
0/0.5 (0) 0/0.3 (0) 11/6.6 (167) 123/33.9 (362)
4,274 Italy
145 England 283 England 3,211 England
Rossiter & Coles 6,292 England [1980] Group 6: Other industrial workers
5.2
5.1
Group 5: Shipyard workers
4.4
Study* (author [year])
Number location
31,150 England
3,070 Germany 665 Germany
6.13 Hodgson & Jones [1986]
6.14 Woitowitz [1986] Subcohort II
Subcohort I
Post-1969
Pre-1969
Low-dose male High-dose male Low-dose female High-dose female
Subcohort
6/8.8 (68) 0/0.9 (0)
1/2.1 (49)
22/11.9 (185)
5/6.34 (79) 3/1.4 (215
24/24.9 14/27.4 (51) (96) 0/0.2 0/0.3 (0) (0)
9/5.8 (156)
ColonGI tract Esophagus Stomach rectum (ICD 150-154)
All GI, incl. meso. 25/23.3 (107) 42/24.7 (170) 4/2.4 (167) 19/10.8 (176) 11/8.1 (136)
All GI, excl. meso.
197/74.2 (265)
102/20.5 (498)
22/15.3 (144) 9/2.6 (347)
57/50.0 (114) 22/10.3 (213)
152/112.1 na (136) na 1/1.0 (96)
108/72.5 (149) 229/78.7 (291) 12/7.3 (164) 117/36.8 (318) 72/26.5 (272)
All cancer
48/29.7 (162) 110/33.5 (328) 2/0.8 (250) 35/4.2 (833) 38/10.7 (355)
Lung
6/2.6 (231)
50/19.4 (532)
Nonmalignant respiratory disease
Observed/expected counts and SMR for various sites
10 10 10
.30 .50 .46
9 9
.31 .31
10
na 185/194.7 (95) 71/40.7 (175)
10
na
834/931.6 (89) 9/9.5 (95)
5
10
.46
10
.33
.34
Cancer proportional mortality Latency
593/355.9 (167)
319/302.7 (105) 499/310 (161) 40/29.1 (137) 234/126.3 (185) 157/103.4 (152)
All causes
From Frumkin, H., and Berlin, J. (1988). Asbestos exposure and gastrointestinal malignancy review and meta-analysis. American Journal of Industrial Medicine, 14, 79-95. b For complete reference, see original source.
a
933 New Jersey
6.12 Seidman [1986]
1,400 England
6.11 Newhouse & Berry 3,000 [1979]; Newhouse England [1985a]; Newhouse [1973] 700 England
Cohort No.
Table VII (Continued)
43
Asbestos-Contaminated Drinking Water
Woodstock Water - 20,000X
Silicon
Iron
Figure 1 (a) Digitized scanning transmission electron micrograph of asbestos fibers collected in Woodstock, New York, drinking water in 1985. (b-e) X-ray maps depicting relative element concentrations. The crocidolite fiber is distinguished by sodium, silicon, and iron while the chrysotile fiber is distinguished by magnesium and silicon.
Line 1-2 34
Measured r-spacing Pixels 200. 200.
Gold-Ring Diameter (X2.355Ä) 471. 471.
Camera Constant Pixel-A 235.5 235.5
Line 1-2 1-3
Measured Pixels 72.1 64.3
Calculated Angstroms 3.27 3.66
Angle 3-1-2
Measured Degrees 45.5
Reference Degrees 44.7
Reference Angstroms 3.271 3.658
Figure 2 Digitized [212] zone-axis electron diffraction pattern from a crocidolite fiber in the Woodstock sample, (a) Unprocessed CCD-camera pattern with 2.355-Ä gold (internal standard) diffraction ring, (b) Processed pattern with measured r-spacings, calculated d-spacings, and reference i/-spacings.
44
Asbestos-Contaminated Drinking Water
analysis. Figures 1 and 2 illustrate TEM-generated characteristics used in identifying chrysotile and crocidolite asbestos in a drinking-water sample. The current EPA methods, published in 1983, requires analysis of all fibers longer than 0.5 /xm and thus is not fully compatible with the EPA's 1991 MCL, which is based on long (>10 μτη) fibers.
ΙΛ
Control
A variety of technologies is available for removal of asbestos from drinking water. Specific applications will depend on the source of the contamination.
A. Natural
Erosion
When source water is contaminated by asbestos from bedrock, conventional treatments utilizing one or several of the sedimentation, flocculation, co agulation, filtration, or equivalent direct filtra tion methods usually remove 95 to 99% of waterborne asbestos if properly optimized. Dredging of asbestos-laden sediments in rivers or reservoirs may also reduce asbestos concentrations in certain situa tions.
B. Deteriorated
AC Pipes
Deteriorated AC pipes often contribute asbestos contamination on a localized level. In several epi sodes, complaints about fibers clogging faucet strainers were the first hints of AC-deterioration problems. Deterioration and resultant contaminant problems may not always be detectable using TEM analysis and the EPA's MCL because of the spo
radic nature of the problem and the fact that more than 95% of waterborne asbestos fibers are usually shorter than 10 μηι. For example, tap water in Woodstock, New York, which had a visible fiber suspension and contained more than 1000 MFL (based on all fiber sizes), was below the ΙΟ-μπιlength-based MCL of 7 MFL. TEM analysis for all fiber sizes and a visual inspection of AC pipes should be part of routine monitoring. In instances where deterioration is caused by cor rosive water, chemical treatments may be applied to reduce the corrosivity. Lime treatment applied in a consistent manner is often effective in reducing acidity, a common promoter of AC-pipe deteriora tion. Chemicals may also be added to form a protec tive lining inside the pipe; zinc salts have proven effective in some cases. Pipes may also be physi cally cleaned and lined with asphalt or rubberized compounds to minimize deterioration. Future con tamination problems can be minimized by following recommended practices when installing or modify ing AC pipe. Finally, AC pipes may be bypassed or replaced by non-AC pipes.
Bibliography Frumkin, H., and Berlin, J. (1988). Asbestos exposure and gas trointestinal malignancy: Review and meta-analysis. Ameri can Journal of Industrial Medicine, 14, 79-95. Schreier, Η. (1989). "Studies in Environmental Science 37: As bestos in the Natural Environment." Elsevier, Amsterdam. Summary workshop on ingested asbestos, (1983). Environmental Health Perspectives, 53, 1-204. Toft, P., Meek, Μ. E., Wigle, D. T., and Meranger, J. C. (1984). Asbestos in drinking water. CRC Critical Reviews in Environ mental Control, 14(2), 151-197. Webber, J. S., and Covey, J. R. (1991). Asbestos in water. CRC Critical Reviews in Environmental Control, 21(4), 331-371.