3
00
r
3
cr
1970 1971 1972 1973 1974 1975
Year
Source: U.S. EPA 1980.
1976 1977 1978 1979
FIGURE 4-6 MAJOR RIVER BASINS WITH ANNUAL AVERAGE NICKEL CONCENTRATIONS
IN AMBIENT WATERS EXCEEDING 100 /j
-------
surface water of Che Adirondack region of New York State were examined
by Lillians et al. (1977) in the sunnier of 1975. Nickel concentrations
ranged from 0.4 ug/i to 14.8 ug/1 in the northern and southern portions
cf sever, lakes. No trend was determined for nickel in the lakes, with
the exception of Ticonderoga Bay of Lake Chanpiain where pollution from
industrial wastes sxisted.
From a review of literature by Bowen (1979), concentrations of
nickel in freshwater form a range of 0.02 ug/1 to 27 ug/1, with a
median of 0.5 ug/1; in sea water the range is 0.13 ug/1 to 43 ug/1,
with a mean of 0,12 ug/1.
4.5.2.2 Effluent Waters
The STORE! system is one of the primary data bases for information
regarding nickel in effluent waters. Since 1977, sampling of nickel
in effluent waters has been recorded for the Northeast, North Atlantic,
and Southeast basins. Table 4-7 shows concentrations of nickel in efflu-
ent waters for the three basins, along with a gross summary. The re-
trievals x^ere of a general nature; neither industry nor plant specific
data was analyzed. For the three areas combined, the maximum concentra-
tion is 400 ug/1, with a mean concentration of 47 ug/1. Overall, the
Northeast has the highest concentrations of nickel in the effluent waters
from year to year.
Samples of nickel were collected near a domestic sewage outfall in
Central Puget Sound, Seattle, Washington (Schell and Nevissi 1977). Con-
centrations of nickel were found to be at or below open sea water values
of 20 ug/1 at three depths, up to 2 m, 50 m, and 100 m.
2.5.2.3 Well Waters
The STORET system serves as the primary data source relating to
nickel concentrations in well water.
Nickel concentrations in well waters are fairly uniform across the
country. In the Ohio River Basin, maximum concentrations of 31,200
and 31,700 ug/1 were reported in 1978 and 1979, respectively.
Typically, the maximum concentration of nickel in well waters did not
exceed 50 ug/1 and the average concentration centered around 10 ug/1;
the average was below the Water Quality Criterion of 13,4 ug/1- Table
4-8 shows, bv niajor basin, nickel concentrations in well waters from
1977 to 1979.
4.5.3 Dissolved and Suspended Matters
Water transport of heavy metals by particulate solids was examined
by Perhac (1974), in eastern Tennessee. The concentration of metals
in the particulates was documented as very high but the quantity of
particulate matter was quite low.
4-26
-------
TA3LE 4-7. NICKEL CONCENTRATIONS IN EFFLUENT WATERS
1977-1979 - STORE! DATA (ug/1)
Major River Basin
Number of
Observations
Maximum Min imum
Mean
Northeast
1977
1973
1979
North Atlantic
1977
1978
Southeast
1977
1979
Gross Analysis
83
79
2
25
31
2
10
233
300
400
100
240
56
52
81
400
0.15
0.12
100
3
5
20
0.12
44
65
100
41
16
29
35
47
Retrieved July 22, 1980.
Source: U.S. EPA 1980
-------
TA3LE 4-8. NICKEL CONCENTRATIONS IX KELL WATERS, 1977-1979 - STORET DATA
(ug/l)a
Major _R_iy_er Basin
Number of
Observations
Concentrations
Maximum Minimum Mean
North Atlantic
32
10
16
Southeast
11
177 0.00
70
Ohio River
59
31,700
3443
Lake Erie
Upper Mississippi
Missouri River
192
19
50 0.13
15
Pacific Northwest
21
Hudson Bav
25
10
Retrieved July 22, 1980.
Source: U.S. EPA (1980)
4-28
-------
Nickel concentrations in dissolved solids at six sampling sites
ranged fron 9000 ug/1 to 45,000 ug/1. The nickel content in coarse
particulatas at the same sites ranged from 35,000 -jg/1 to 110,000 ug/1.
The largest percentage of nickel was uncovered in dissolved solids as
opposed to particulate solids, being at least 73% at five sampling sites
(the sixth site was considerably lower).
Table 4-9 displays the documentation of nickel concentrations in
dissolved and suspended matters, as reported from STORE!, for most
major basins from 1977 to 1979. For the nation as a whole, maximum
and average nickel concentrations in dissolved matters are 1000 and
24 ug/1, and for suspended matters, 1400 and 13 ug/1.
4.5.4 Sediment
The transport of heavy metal in bottom sediments was examined in
the waters of eastern Tennessee to define the distribution of heavy
metals in a fluvial system (Perhac. 1974). MicUel was one of eight
heavy metals measured in a stream located in an industrialized urban
area, in a stream which flows over exposed carbonate rocks containing
zinc minerals, and in a stream located in a rural non-mineralized area.
The quantity of heavy metals in bottom sediment varied considerably
from sample to sample. Detailed analysis of bottom sediment samples
from Joe Mill Creek and the Tennessee River was conducted. Generally,
the concentrations of nickel increased with decreasing grain size,
. as shown in Table 4-10.
Samples taken from bottom sediment in the Tennessee River near
Knoxville indicate that more nickel was present than in Joe Mill Creek,
possibly because of petroleum wastes from many diesel vessels using
the river. In Joe Mill Creek, the nickel content in bottom sediment
ranged from 20,000 ug/1 to 64,000 ug/1, compared to the range of 39,000
ug/l to 109,000 ug/1 in Tennessee River bottom sediment. The higher
levels of nickel in bottom sediment did not have an impact on the con-
centrations of nickel in surface waters, which were low at both sites.
Knauer (1977) determined the immediate impact of a new Australian
nickel refinery on sediment metal levels in Halifax and Cleveland Bays,
Australia, which is discussed here as a basis for comparison. Slightly
higher levels of nickel appeared in the Queensland Nickel outfall adja-
cent to the refinery than at either Halifax or Cleveland Bays. The
average concentrations (ug/g dry weight) of nickel in surface and sub-
surface sediments (>10 cm) for Queensland Nickel was 14 and 12 ug/g,
Halifax Bay 11 and 11 ug/g, and Cleveland Bay 9.3 and 8.8 ug/g. Supple-
mental laboratory experiments suggested that the future levels of nickel
in sediment would increase as a direct result of the new nickel refinery.
1-29
-------
TABI.K 4-9.
I
(*)
o
NICKEL CONCKNTKAT[ONS IN DTSSOI.VKI) AND SUSI'KNDKD MATTKKS
KROM MA.10K lilVKR BASINS, 1977 to 1979 - STOKIJT DATA
(IUS/O
Major River Basins
Northo.Tst:
North Atlantic
Southeast
Tennessee River
Ohio Kiver
J.ake Erie
Upper Mississippi
Lake Michigan '
Missouri River
Lower Mississippi
Colorado River
Western Culf
Pacific Northwest
California
Great Basin
Lake Huron
Lake Superior
CROSS ANALYSTS
Dissolved Matter
Suspended Matter
Ohservat ions
3S
218
387
107
195
861
175
24
380
533
193
38
30
80
261
3
5
Maximum
35
100
470
100
800
1000
83
290
22
50
35
75
•:,
?00
200
9
1
Me a n
2
72
69
94
55
8
14
31
3
/
••l
3
•\
0.7
56
13
*j
0.4
Observations
31
18
99
7
23
1
127
1.1
193
439
116
35
25
30
18
3
5
Max i mum
11
22
36
17
26
0
50
7
440
.180
1400
16
26
50
8
3
2
Mean
1
5
4
4
5
0
15
2
19
11
39
4
4
8
3
1
0.8
3525
1000
1181
1400
13
Retrieved July 22, 1980.
Source: U.S. EPA (1980)
-------
TABLE 4-10. NICKEL CONTENT -IX BOTTOM SEDIMENT SAMPLES
Nickel Content (rag/1)
Composite
Joe Mill Creek Total
Sample
Sample
Sample
1 12-32
2 12-31
3 52
<0.2
82
108
99
Size Fraction (
0.2-2 2-5 5-50
83
.87
187
70
75
66
31
28
43
u)
50-100
27
27
41
>100
<30
<28
60
Tennessee River
Sample
Sample
Sample
Sample
1
2 —
3
i
186
227
135
220
108
150
90
23"
39
208
59
271
69
69
50
90
30
50
30
89
50
20
40
30
— indicates not available
Source: Perhac (1974)
4-31
-------
Concentrations of nickel were measured at several depths in sedi-
ment at various lakes of the Adirondack Mountain region of New York
State (Williams, et al.). Nickel concentrations in surface and sub-
surface sediments (10 to 20 cm) were analyzed for seven lakes. Con-
centrations in surface sediments ranged from 0.2 iag/g to 5.0 ug/g and
from 0.1 ug/g to 2.9 ug/g in subsurface sediment. Lakes with higher
nickel concentrations were subject to pollution from industrial wastes.
Levels of organonetallic nickel were determined in sediment by
Nakamura and Kashimoto (1979). Heavy metals in crude oil reach sedi-
ment as a result of oil pollution in the sea environment. From three
sediment samples taken in Osaka Port, the levels of organometallic
nickel (dry matter) were 0.218 yg/g, 0.149 Mg/g, and 0.180 ug/g.
N'ickel in sediments has been documented by Bowen (1979) from
literature as 225 LZ/g in marine clay, 30 ug/g in marine carbonates,
and mean levels of 58, 7, 9, and 52 vg/g in shale, limestone, sand-
stone, and sediment, respectively.
Nickel concentrations in sediment have been recorded in fourteen
of the continental major basins. During the three-year period of
1977 to 1979, maximum concentrations of nickel in sediment ranged
from 20 to 1200 '-g/g and mean concentrations from 4 to 172 ug/g.
These results are consistent with findings in the literature. Nickel
concentrations in sediment are displayed in Table 4-11 for the reporting
basins and in the United States. In general, nickel concentrations
in sediment are two to three orders of magnitude higher than nickel
concentrations in ambient waters. Figure 4-7 presents concentrations
of nickel in sediment for the nation from 1971 to 1976. The heaviest
shading represents concentrations exceeding 25 ug/g. Sampling since
1976 indicates basically the same conditions, with expansions to the
western section of the country.
4.5.5 Air
4.5.5.1 Industrial Areas
Emission data with respect to nickel have been documented for
several emission categories, including mining, metallurgical, fuel
combustion, waste incineration, secondary metal industry, consumptive
uses, and processing and utilization. Table 4-12 exhibits the emission
factors for nickel from these industrial categories.
Other emissions of nickel have been documented (Schroeder
1962). Fly ash from residual fuel oil used in power plants and in
heating large office buildings, apartments, and schools has 1.8 to
10% nickel oxide. Fly ash crude oil used in the facilities contained
55 ug/g, and asphaltene fraction 245 ug/g. Particulates from municipal
incinerators in Milwaukee have 1 to 10% nickel.
i-32
-------
TABLE 4-11. NICKEL CONCENTRATIONS IN SEDIMENT,
1977-1979 - STORE! DATA3
Number of Concentrations
Major River Basins
Northeast
North Atlantic
Southeast
Tennessee River
Ohio River
Lake Erie
Upper Mississippi
Lake Michigan
Missouri River
Lower Mississippi
Colorado River
Eastern Gulf
Pacific Northwest
Lake Huron
Observations
58
69
172
10
22
247
4
22
33
37
15
117
27
6
Maximum
200
360
80
39
50
290
20
1200
120
40
20
63
238
23
Minimum
5
1
7
7
10
1
5
1
0.00
0.00
0.00
0.5
4
5
Mean
18
29
12
16
24
37
11
172
18
14
4
14
47
15
GROSS ANALYSIS 839 1200 0.00 27
Retrieved July 22, 1980.
Source: U.S. EPA (1930)
4-33
-------
Legend:
Cone.
blank No Data
m o
"/#%
9 >°-12
M 12-26
All & I'•-•!>*
No. Cells
24
42
43
38
J U.S. 147
v.,/--^
./
^
V *
0.09
18.94
Miles xlO
-^ 56.83 »•"
Source: U.S. EPA 1980.
FIGURE 4-7
-------
I'AHI I-! 1-12. HUSSION I'ACTOKS I-'OU NICkKI. I'lfllM INIIIISTKIAI SlIIIHCr.S
KM I SSI I IN J^ACTIIK SlHIKCK KMISSJUN I ACTOIt
Mlninit .mil Mclal lnri;lcal 'J k);/|OJ k); of nickel produced l-'orel)>n crude nils
I'lon-sslilK of Nickel '< kn/1"1 kit of nickel i-liari-cd Miino)tas crnde, Venezuela 0.04 k|'/lo' liters
Si.link-.s sli. I II.J k|t/IO k|t of stainless steel |>roilnce.l Crude oil, Vene/ncla O.OOli kf./IO1 liters
Niikel alloy steel 'i ku/IO1 k|\ of nickel charged Nigerian crude oil O.OO7 kit/Ill1 liters
lion ami sli.-l sera). O.OOOH kit/101 kit ol sleel ami iron lol.o . rude, I'nerlo nr.l,/.. 0.0'j kit/101 HUTS
Niikel alloys I k|*/|0^ k|t of nickel charged Venezuela
Copper I,asc alloys I k|t/|O* k|; of nickel ili.iif.L-,I A,;u.isav crmle oils, Venc.;iie la 0.002 kit/101 liters
I Ic.irlcal alloys I kj;/|0 kr of nickel cliar|.,ed Avcraue for l'orel|'ii crude oils 0.02 kn/IO1 liters
Casi lion III kit/ IU ' k|t of nickel charged ,. . „,,,,,,
,' 1 . ' , . . . lorelitn lies I dual Dl Is
H.uu.ies ', k,S/ll) k,; of nickel n.oc.cs.sed /M, fnel oil. Viritln Isl s 0.0) k,;/10' 11 UTS
I,.|»eul I'l s: liry Truces* Hl> fuel oil, VeneziH'la O.IK (O.OIK toll.Oli) k|t/IO liieis
Kiln 200 kr./UI k|; ot feed ("i fuel oil, Arnl>.i, N.A. 0.01 k|t/IO liters
lee.I lo raw M||| 5 k(;/H>3 k|; of feed IK- fuel oil, Si. Crolx. VI 0.01 kit/Ill* llteis
,Mi ..|..n,ilor all, i raw will 0.5 kit/Ill1 kg of feed # clinker cooler (exit f i, HI, 100 k|t/IOJ k|t of feeil Conum-rclal nulls «S 0.007 k|;/lo' lilers
*~" iu,, 1,.1,-liouses) Coiimieririal nulls ("i O.OOu kit/101 liters
riiiishiii,; mill alter air separator 2 kit/101 kr of feed ,. ,..
i: -'"- '-•» "-2 k'^|(l k'- '••"' •»"'' ""MuUiMe'hearll, "" '' '"" 0.002 k,./lo' k,t of solid „.,„,, in. Hi.-, a, ed
l',«ji-l I'l.ml SUldy I I ill.11 :-..•,! I,, ,1 0.0002 k|-,/lo' I -j. ol solid wasle i u. in, I al ed
South Carolina II.1111(11 (O.OOO.' lo 0.0005) k|,,/lo' .. . . , , .
. 'lnnlciii.il Incinei.iior
O.OOOno.OOoTu. 0.000-,, •.,../••.» K.fnse o,,lv O.02 k«/.0 | k,t o, sol, d ,,,s,e m.ine.a.ed
llrfuse and slndite 0.001 ku/|OJ ki; of solid wasle In. Inei aled
k|t coal linrncd
Illinois O.OOO2 kr./Kt k|> coal I,urn.:,I l.uln il al in,'. Oil O.IIOK Kit/Ill' liters ol Inl.rl.al In,- oil
Kansas O.OIHI1 (0.0002 lo O.OOOS) kft/IO1
k|t coal hnrned
I in-1 C.Hiiliusl Ion III I
U.S. Crude, ill I:
lex.is O.OO2 (O.OOI I o II.(Ill',) kit/101
I iters crude oi I
0.002 ki-,/101 liters
O.OO1) k|t/Ml) liters
UvoiHlnit O.OO2 kit/Ill1 lilers
c.illloinl.i O.Obkit/IO1 liters
Alaska 0.01 k|>,/IO^ liters
Av.-r.ir.e lor U.S. crude oils 0.01 k|;/ III' I i I ers
Aver.,)-,' lor im|,oi l.-.l cmde oils O.OO'J kit/IO1 liters
Sonice: Anderson (
-------
Sullivan (1969) documented concentrations of nickel near the
Alloy Products Division of the International Nickel Company, Inc. in
Hunting ton, I-.'est Virginia, as 1.2 ug/m3. Concentrations at six other
sampling stations in the Ironton-Ashland-Huntington Valley were lower,
at 0.04 ug/m3.
In the heavily industrialized city of Glasgow, Scotland sites were
selected to construct a comprehensive view of the atmospheric conditions
with respect to airborne metallic pollutants (McDonald and Duncan 1978).
Sample sices were located in residential areas, some distance from polluting
sources, in the vicinity of shipbuilding, iron and steel, and coal-
burning power station operations, and in close proximity to main
thoroughfares. The range and mean values of 11 metals, including
nickel, were documented, and compared with values reported for other
urban areas. In general, mean values were in agreement with those
for other areas. However, the mean value (128 ne/nH) reported for
nickel, in particular, was higher by a factor of 2 than values reported
in Chicago (60 ng/nP) and Galnorgan, Wales (65.6 ng/m^) , and higher
by a factor of 12 when compared to results from 50 stations in Texas
(10 ng/m3).
In Wollongong, Australia, significant correlations were found
between distance from copper smelter and heavy metal contamination
of vegetables and soil in domestic gardens around the smelting complex
(Beavington 1975). Specifically, in a garden only 150 meters from the
main chimney 6 ug/g of nickel was reported in the leaf of a mature
flowering plant. Twenty-one samples of leaf vegetables were collected
from 17 gardens, along with soil samples up to 10 cm. Mean levels of
nickel calculated at dry matter weight for lettuce, other leaf
vegetables, chilies, and soil were 2.7 ug/g, 5.0 ug/g, 0.9 ug/g,
and 1.05 ug/g, respectively.
4.5.5.2 Urban Areas
The presence and concentrations of several airborne metallic pol-
lutants were surveyed in 58 cities (Schroeder 1962). Nickel
was detected in 56 of the cities, forming a range of 1 ng/np to
118 ng/m^. The cities polluted heavily with airborne nickel, with
concentrations ranging from 30 ng/ia to 120 ng/m , include New
York City and Rochester, Mew York; Bayonne, New Jersey; Portland,
Oregon; Somerville, Massachusetts; New Haven, Hartford, and Bridge-
port, Connecticut; Bakersfield, Burbank, and San Bernardino, California;
and Baltimore, Maryland.
Seasonal changes exhibited variations in mean nickel concentrations
in ten cities. During colder months, the mean concentration of nickel
was documented at 44 ng/ro^ compared to 26 ng/rn-3 in warmer months.
This is attributed to an increased use of petroleum and coal in the
colder months.
4-36
-------
The dry deposition of toxic trace metals u-as studied in N'ew Yorl:
City beginning in 1972 (Kleinrr.an §_t al. 1977) . l-.'eekly samples of
suspended particulates and monthly fallout samples were collected for
12 metal elements by atonic-absorption spectrophotometry at four
locations. The results of average nickel dustfall and ranges of
monthly nickel concentrations for three stations were:
D-. month
Station Location Average Range
Bronx 400 14-2500
Lower Manhattan 400 33-3200
XI d town Manhattan 300 64-1900
Sullivan (1969) documented concentrations of nickel in the urban
atmosphere ranging to a maximum of 690 ng/ra^ with an average of 32
in a 1964 national sampling survey.
4.5.5.3 Rural Areas
Documentation of nickel concentration in the rural atmosphere is
very limited. A survey of airborne metallic pollutants, including
nickel, was conducted in 29 non-urban areas (Schroeder 1971). In 28 of
the 29 areas, concentrations of nickel in the air were documented as a
range of 6 ng/nH to 12 ng/m^. In the 29th area, it was undetected.
4.5.6 Soils, Rocks, and Plants
About 0.008% of the earth's crust is nickel, with the largest
portion, approximately 0.01 %, in igneous rocks (Nielsen et al. no date)
Of the igneous rocks in the lithosphere , the ultramafic rocks are
abundant in nickel — 140 ug/g in gabbro to an average of 2000 ug/g
in peridotite. Diorite contains roughly 4Q ug/g of nickel and granite
rocks 8 'Jg/g. An average of approximately 50 ug/g of nickel is
found in sedimentary rocks, shale, and carbonate rocks.
In plant tops, the average range of nickel concentrations is 0.05
ug/g to 5 '.g/g , dry weight. Nickel concentrations in plants materials
used as food are shown in Table 4-13.
Contamination of roadside soil and vegetation near roadways used
by motor vehicles was studied (Lagerwerff and Specht 1970). Sites were
selected on level areas near four heavily trafficked roads — U.S. 1 at Belts-
ville, MD, Washington-Baltimore Parkway at Bladensburg, MD, 1-29 at Platte
City, MO, and Seymour Road north of Cincinnati, OH. Soil samples were
collected at distances of 8, 16, and 32 in from traffic and at depths
of up to 5, 10, and 15 cm. Results (shown in Table 4-14) indicate that
concentrations of nickel in soil and vegetation decrease with distance
from traffic and with deoth.
4-37
-------
TABLE 4-13. NICKEL CONCENTRATIONS IN FOODSTUFF
ITEM
GRAINS
Wheat
Bread, whole wheat
Cereals
Oats
Rice
VEGETABLES AND FRUIT
Potatoes
Peas
Beans
Celery, fresh
Swiss chard, Chicory, Spinach'
Escarole
Lettuce, head
Lettuce, organic
Cabbage
Watercress
Tomatoes
Tomato Juice, canned
Broccoli
Carrots
Mushrooms
Onions
Apples
Bananas
Pears
Figs
Plums
Apricots
Oranges
CONCENTRATION
Wet Weight
(ug/1)
0.16-0.74
1.33
0.13-3.00
1.71-2.60
0.30-1.803
0.56
0.30-1.66
0.17-2.59
0.37
0.27-0.71
0.14
1.14
0.14-0.32
0.02
0.05
0.33
0.08
0.34
0.20
Dry Weight
(ug/g)
0.34-35
0.45
0.02b
0.08-0.37
2.00-2.25
0.59
2.40
1.51
3.30
0.13
0.01-0.15
0.30
3.50
0.16
0.90
1.20
0.90
0.64
0.16
Rice sampled includes polished, unpolished, and puffed.
Vj
Polished rice.
Source: Nielson et al. (no date).
4-38
-------
IA3LE 4-14. CONTAMINATION BY NICKEL OF ROADSIDE
SOIL AND VEGETATION
Nickel in Soil Profile Layer, cm
Meters C
Site
Meters
From Road
Beltaville,
8
16
32
Grass (%ig/g -
dry weight)
MD
5.
3.
2.
0
3
3
0 -
5
0
- 10
10
- 15
(yg/g - dry weight)
4.
2.
2.
7
4
2
1
0
0
.00
.90
.62
0
0
0
.81
.60
.59
Washington-Saltinore Parkway at Bladensburg, MD
i
8
16
32
3.8
2.5
1.3
7.4
4.4
2.4
5.6
1.6
1.2
1.40
0.79
0.57
Source: Lagerwerff and Specht (Iy70)
4-39
-------
In a review of literature, Bowen (1979) documented the median and
range of nickel in soils at 50 ug/g and 2 to 750 ug/g, respectively.
Documentation for nickel levels in minor sedimentary- rocks (in ug/g)
includes: manganese modules - 4900; phosphorites - <2 - 1000; petroleum
10; and coal - 10 (mean) and 1-SO (range).
4.5.7 Biota
Documentation of nickel concentrations in biota in the STORET
system reports maximum values ranging from 3 ug/g to 35 ug/g (dry
weight) for shellfish and mean values 0.71 ug/g to 8 ug/g. Maximum
concentrations in fish tissue range fromO.13 ug/g to 27 ug/g (wet
weight) and mean concentrations from 0.11 ug/g to 3 ug/g. Concen-
trations of nickel in shellfish and fish tissue for major river basins
are presented in Table 4-15.
Heavy metals in crude oil are frequently a source of contamination
for marine products as oil pollution in the sea environment occurs.
Nakamura and Kashimoto (1979) determined the levels of organoraetallic
nickel in the hexane extracts of marine products from Japan. Table 4-
16 exhibits the levels of organctnetallic nickel in marine products; the
highest level of organometallic nickel appears in Turban shell intestine
(0.063 ug/g) at Ishikawa, Japan.
4.5.8 Summary
Nickel has been detected in ambient surface waters of the United
States at concentrations varying from <1 ug/g to 100 ug/1, with approxi-
mately two-thirds of the detections in the range of <1 ug/1 to 10.0 ug/1.
Ambient concentrations exceeding 100.0 ug/1 have occurred at different
times in various major river basins throughout the country, although
most recently (1978, 1979) the Ohio River Basin has consistently had
higher levels of nickel. The mean concentration of nickel in well
waters is 10 ug/1, which is below the established human health criterion
level for waters of 13.4 ug/1. However, higher levels of nickel were
detected in well waters within the Ohio River Basin in 1978 and 1979.
In stream sediments, the concentration of nickel tends to increase as
sediment grain size decreases. More significantly, however, the nickel
concentration in stream sediment increases greatly in areas near indust-
rial discharges. Nickel occurs in air at concentrations up to an order
of magnitude higher in urban and industrialized areas (1 to 690 ng/m^)
than in rural areas (6 to 12 ng/m^).
Although nickel occurs naturally in the earth's crust and can be
found at low concentrations in all of the environmental media, the
highest concentrations detected in air, water, suspended sediments,
and plants tend to be associated with industrial and urban activities.
Concentrations of nickel in the environment are summarized in Table
4-17 from the primary data sources detailed in this section.
4-40
-------
TABLE 4-15. CONCENT RAT IONS OF NICKEL IN SHELLFISH .AND FISH T ISSUE
D
MAJOR 3ASIN
Northeast
North Atlantic
Southeast
Ohio River
Lake Erie
Upper Mississippi
Lake Michigan
Missouri River
Lower Mississippi
Colorado River
Western Gulf
Pacific Northwest
California
Great Basin
Lake Huron
Lake Superior
Alaska
Hawaii
GROSS ANALYSIS
SHELLFISH FISH
drv weight vet
•-' Obs. Max. Mean » Obs.
17 35 8 524
32 4 2 218
-b 8
- 42
_ 110
_ 9
_ 140
_ 11
- 5
_ 17
23 7 3 8
19 3 0.71 45
13 4 2 21
2
142
140
6
18
TISSUE
weight
Max .
27
6
i
10
8
0.13
0.50
0.43
13
*_
10
5
5
5
3
0.50
1
8
Mean
0.70
0.32
0.57
2.00
0.45
0.11
0.26
0.13
3
2
3
1
1
3
0.41
0.14
0.58
1
104
35
1466
0.59
Retrieved Julv 22, 1980.
[^
Major basins wichoue entries (shown with -) indicate no reported detections,
Source: U.S. EPA (1930)
4-41
-------
IA3LE 4-16. ORGANOMETALL1C NICKEL IN THE HEXAME
EXTRACTS OF MARINE PRODUCTS FROM JAPAN
Marine Product
Clan (Meretrix)
Short-necked clams (Tapes)
Corbicula (Corbicula)
Turban shell (Turbo)
Scallop (Pecten)
Ear shell (Kaliocis)
Ark shell (Area)
Oyster (Crassostrea)
Cella stearnsii
Source
Ehime
Ehime
NVUSVU
Korea
Mie
Shizuoka
Mie
Shimane
Ishikawa (shellfish)
Ishikawa (intestine)
Yamaguchi
Aomori
Aomori
Tokushioa
Mie
Hiroshima
Hiroshima
Hiroshima
Hiroshima
Osaka
Qrganometallic N'ickel
(pg/g)
0.010
0.005
0.003
0.001
0.004
0.004
0.003
<0.001
0.017
0.063
0.017
0.008
0.004
0.014
0.019
0.003
0-027
0.005
0.016
0.013
Source: Nakamura and Kashimoto (1979)
4-42
-------
TABLE 4-17. CONCENTRATIONS OF NICKEL IN THE ENVIRONMENT
Media/Biota
Ambient waters
Well waters
Effluent waters
Nickel Concentration
0 to 100 ug/1, typically
50 ug/1 - maximum; 10 pg/1 - mean, typically
400 pg/1 - maximum; 47 ug/1 - mean
Sediment
1200 ug/g - maximum; 27 ug/g - mean
Dissolved matter
Suspended matter
Urban Atmosphere
Rural Atmosphere
1000 ug/1 - maximum; 24 ug/1 - mean
1400 ug/1 - maximum; 13 ug/1 - mean
1 to 690 ng/ra3
0.6 to 12 ng/m3
Soils
Rocks
Plants (tops)
0.57 to 7.40 ug/g (dry weight)
2 to "50 ug/g
0.05 to 5 ug/g (dry weight)
Biota
Shellfish
Fish Tissue
35 ug/g - maximum; 3 ug/g ~ mean
(dry weight)
27 pg/g - maximum; 0.59 ug/g - mean
(wet weight)
Note: These nickel concentrations provide a range of values that
were discussed in the text of this chapter.
4-43
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4.6 SUMM.ARY
Two important conclusions can be reached from the information on
environmental fate, biotic fate, and monitoring presented in this chapter.
First, low, natural background levels of nickel are present in all parts
of the environment. Second, elevated concentrations of nickel appear
to be fairly restricted to localized areas which are associated with
industrial activity and the urban environment, particularly in sedi-
ments.
Physically, chemically, and biologically degrading processes cause
nickel to be eroded and deposited in waters (ambient, effluent, and
well), stream sediments, soils, air, and biota. Generally, these con-
centrations are quite low. Typical ambient and well waters contain nickel
in the range of 5.0 to 10.0 ug/1 and effluent waters have an average of
47 ug/1 nickel. Sediments and dissolved and suspended stream matter
have mean concentrations of nickel between 13 ug/1 and 27 pg/1. Soils
have concentrations ranging from 0.57 ug/g to 7.40 ug/g, with rocks
somewhat higher. Plant levels are commonly below 1.0 ug/g. The back-
ground levels of nickel in the non-urban atmosphere are generally
between 0.6 ng/m^ and 12 ng/m^. These levels remain consistently
low throughout most of the natural environment.
There are a number of industrial and urban activities utilizing
large quantities of materials which contain nickel. Fossil fuels are
possibly the most significant natural resource or product used in the
United States which contain nickel and consequently release large
quantities of nickel to the atmosphere. The activities associated
with the use of petroleum and coal directly and indirectly affect the
nickel concentration in all of the environmental media through pro-
cesses such as fallout, runoff, and plant uptake. There are other
industrial and urban activities which release nickel to the environ-
ment, including the manufacture of cement, alloys, and iron and steel;
sewage treatment and sludge incineration; and municipal incineration,
particularly of nickel-bearing materials. It is in locations where
these activities are intensified that the nickel concentrations become
elevated.
Because a major portion of the releases are atmospheric, air becomes
the environmental media with the highest initial concentrations of
nickel. The other media are indirectly affected by atmospheric trans-
port of nickel and consequently areas experiencing high atmospheric
release of nickel are likely to experience high nickel concentrations
in the surrounding soil, water, and vegetation.
4-44
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-------
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4-49
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5.0 EFFECTS AND EXPOSURE — HUMANS
This chapter discusses the human effects of exposure which have
been studied, considers the established water quality criterion for
humans, and presents dose-response extrapolations. The routes of exposure,
by inhalation and ingestion and through percutaneous (dermal) exposure,
are identified and quantified within the limits of the available data.
5.1 EFFECTS
5.1.1 Introduction
Nickel is thought to be an essential tnicronutrient since it nearly
satisfies certain criteria for essentiality of trace elements. It
appears, however, that no human disease states have been attributed to
a nickel deficiency and experiments in animals support this conclusion.
It seems quite unlikely that nickel deficiency could be a problem in
human nutrition since its presence in the environment and diet is so
ubiquitous. The NAS monograph (1975) discusses the essentiality of
nickel in considerable detail.
Of far greater concern is the determination of levels of nickel
exposure, by various routes, that are hazardous to human health. This
is a particularly difficult task. While the "background" level of expo-
sure to nickel through ingestion, inhalation, and skin contact has not
been shown to be particularly hazardous, certain nickel compounds,
especially nickel carbonyl, are clearly toxic. Most nickel compounds
are toxic only at elevated doses via routes of entry to the body that
permit high concentrations of nickel to be acheived ac the cellular or,
more importantly, at the subcellular level.
The crucial consideration for assessing the risk of nickel toxicity
is whether or not nickel can be absorbed and then reach the susceptible
sites in the organism. This depends on the exposure route and the physico-
chemical form of the nickel. It can be understood then that nickel car-
bonyl is especially toxic because its combination of volatility, lipid
solubility, and chemical stability permit rapid absorption by most
routes into Che organism, and subsequent wide extracellular and intra-
cellular distribution. Intracellular decomposition and oxidation to N
exposes sensitive subcellular processes to nickel ion. Thus, nickel
carbonyl is a near ideal carrier for nickel, circumventing most of the
protective mechanisms and barriers of the body. In contrast, orally
ingested nickel salts have low toxicity because they are poorly absorbed
and that which is absorbed is rapidly excreted from the body. High levels
of nickel in the diet or drinking water of experimental animals are
tolerated with minimal effects.
The major area of concern is toxicity from inhalation of nickel
compounds. A number of studies and several recent reviews have indicated
that nickel-refinery workers are at increased risk of developing respi-
5-1
-------
ratory tract cancer. The role of nickel in the development of respiratory
tract cancer is not clear, however, because these workers were also
co-exposed to other suspected carcinogens (e.g., asbestos and poly-
cyclic aromatic hydrocarbons). Also, the risk to nickel workers of
developing respiratory trace cancer has declined because of greatly
improved industrial hygiene which has reduced exposure to most if
not all of the toxic and carcinogenic compounds. The use of retrospec-
tive epidemiological data to compute risk in terms of a dose-response
relationship is virtually impossible because little or no quantification
or speciation of the various nickel compounds is available.
Animal studies indicate that nickel carbonyl and nickel subsulfide
are carcinogenic by the inhalation route. These and some other nickel
compounds cause adverse lung pathology and have been shown to alter
lung "cleansing" processes, such as muco-ciliary clearance and alveolar
macrophage activity. In vitro assays tend to support the in vivo
carcinogenicity results for certain nickel compounds.
Other areas of concern to the risk assessment are discussed in
this section. Briefly, it has been reported that nickel carbonyl was
found to be both1 teratogenic and fetotoxic in animal studies; high
levels of nickel in drinking water or diet had adverse effects on
neonates (newbornes) in animal studies; and nickel contact dermatitis is
prevalent in humans but probably not life-threatening.
5.1.2 Pharaiacoklneti.es
The major routes of exposure of man to nickel are via ingestion
(food and water) and inhalation. Parenteral absorption (intravenous,
intraperitoneal, subcutaneous, etc.) is not of importance in human
exposure except, possibly, in the case of internal metal prostheses.
Percutaneous absorption is minimal, but is important in connection
with nickel allergy.
The extent and rate of absorption by any route varies widely with
the physicochemical form of nickel. Variable lipid and water solubil-
ities, chemical stability of the specific compounds, and their variable
tendency to interact with other molecules in vivo practically preclude
any useful generalizations about nickel absorption unless the chemical
form of the nickel is specified. These considerations must be taken into
account again when evaluating bio-distribution, metabolism, and elimination
from the body.
5.1.2.1 Absorption
Ingestion of nickel is on the order of 500 ug/day in humans and
almost all of this is excreted in the feces without being absorbed.
According to several studies cited in the EPA criterion document (U.S.
EPA 1979), 1 to 10% of dietary nickel is absorbed. Even when the Ni
ion was incubated in a dilute acidic solution such that interaction
with foodstuffs was largely avoided, only 3 to 6% of the dose was absorbed,
regardless of the size of the dose (Ho and Furst 1973).
5-2
-------
Korak and Sundeman (1973) found that fecal excretion of nickel by
healthy human subjects was on average 100 times greater than urinary
excretion. Thus, fecal excretion can be used as a Treasure of nickel
ingestion.
Distribution and metabolism studies indicate that absorbed nickel
(Mi"*""*") is primarily excreted in the urine not into the bile and con-
sequently the faces (Onkelinx et al.- 1973) ; thus, it can be concluded
that inorganic nickel compounds as are found in food and water are not
absorbed to a significant extent and that entero-hepatic circulation
does not explain fecal excretion of ingested nickel.
Inhalation is the most important route of exposure to nickel com-
pounds from the standpoint of adverse health effects. The respiratory
tract is both a point of entry to the rest of the body for toxic air
pollutants and a site of toxic response. Typically, soluble aerosols
and gases can pass through the lung epithelium into the blood in which
they are transported throughout the body. Insoluble particulates
tend to be deposited on the epithelium along the respiratory tract
and may be retained in the lung for a much longer time. Whether or
not a compound passes through or is retained by the lung markedly
affects the nature of the effects.
The International Radiological Protection Ccnmissior. Task Group
on Lung Dynamics (IRPC 1966) has formulated detailed deposition and
clearance models for inhaled particles. Deposition of the particles
along the respiratory tract depends on particle size, density, hygroscopic
properties, breathing rate, and whether breathing is via mouth or nose.
Figure 5-1 and 5-2 indicate the predicted deposition in three respi-
ratory tract zones as a function of aerodynamic diameter (unit density
assumed) and at two breathing rates. Figure 5-1 indicates that at near
resting breathing rates very small particles (^0.5 urn) are retained
to a minimal degree. It is known, however, that these small particles
penetrate farthest into the small airways and alveoli of the lung.
Larger particles tend to deposit in the upper respiratory tract,
especially the nasal passages. During mouth breathing, a greater
fraction of inhaled particles are deposited in the lungs, although large
particles are still deposited in the mouth- and oropharynix (IRPC 1966).
Clearance of particles from the lung depends on many factors
including aqueous solubility, depth of penetration into the respira-
tory tree, and interaction of the particles with the tissue. Clearance
mechanisms include dissolution, muco-ciliary transport, and endocytosis.
Experimental work on the absorption of nickel compounds via inhala-
tion has been done almost exclusively in animals. Interpretations with
respect to human inhalation ara not straightforward. There are signif-
icant differences in breathing dynamics between hunans and laboratory
rodents. For example, rats and mice are nose breathers exclusively,
while breathing in humans is through both nose and mouth. However,
these experiments are illustrative of the variability in absorption,
retention, and clearance of the different nickel compounds.
5-3
-------
34567
Aerodynamic Diameter
10
Source: IRPC (1966).
FIGURi 5-1 DEPOSITION AS A FUNCTION OF PARTICLE SIZE FOR 15
RESPIRATIONS/MINUTE. 750 cm3 TIDAL VOLUME
100
Pulmonary
N
Tracheo-bronchia
34567
Aerodynamic Diameter (Mm)
Source: IRPC (1966K
FIGURE 5-2 DEPOSITION AS A FUNCTION OF PARTICLE SIZE FOR 15
RESPIRATIONS/MINUTE, 2150 cm3 TIDAL VOLUME
5-4
-------
".-."ehner and Craig (1972) exposed Syrian golden hamsters tc nickel
oxide (NiO) or cobalt oxide (CoO) dust in concentrations ranging
from 2 -g/1 to 160 ug/1 (mg/rn^), having particle sizes of 1 to 2.5
un (aass median aerodynamic diameter). Approximately 20% of the
inhaled dose of NiO was deposited in the lung as determined after
acute, 3 week subacute, or 3 month subacute exposures. Their data
(from Figure 5 in Wehner and Craig 1972) was replotted as loge (per-
cent of maximum NiO deposited in lung) versus time after the end of
the exposure. This plot suggests an initially rapid clearance phase
(half-life %2-5 days) followed by a much slower clearance phase between
3 and 170 days with a half-life of 84 days. In contrast, cobalt oxide
(CoO) particles were rapidly cleared from the lungs of Syrian golden
hamsters after exposure to CoO dust; the clearance half-life was about
1 day (Wehner and Craig 1972). Histological examination of the lungs
showed accumulation of NiO particles in the lung, occasionally com-
pletely filling some of the alveoli. Particles were also noted to
be phagocytized (i.e., engulfed) by alveolar rnacrophages.
Similarly, high lung retention and slow clearance of a nickel-
enriched coal fly ash (NEFA) were reported by Wehner et al. (1979b).
After 2 months of exposure to NEFA at 188 mg/m^, 6 hours/day, 5 days/
week or to fly ash (FA) at 183 mg/ra , the hamster lungs were heavily
laden with dust particles. At the end of exposure there were approximately
78 yg/Iung of NEFA for a retention of about 50% (assuming 60 ml/nin as
the average minute volume of the hamster during exposure). The lungs
of hamsters sacrificed 30 days after the end of the exposure contained
a similar amount of NEFA, indicating that the dust was not readily
cleared. There were no major histopathological differences among
NEFA, FA, or control lungs except for the accumulation of dust in
both NEFA- and FA-exposed hamsters. Chronic inhalation studies were
reported to be underway.
In contrast, nickel was rapidly cleared from the lungs of mice
exposed to NiCl2 aerosol (<_ 3 yn diameter, 644 pg Ni/m^) for 2 hours.
The clearance was exponential with a half-life of ""3 days (Graham
et_ al. 1975).
These studies indicate the variable results on the clearance of
inhaled metal salts. While a difference in aqueous solubilities
between NiO and NiCl? may help explain the differences in clearances
(the readily water-soluble NiCl2 is rapidly cleared), other factors
must contribute to the differences in CoO and NiO clearances, since
both compounds are relatively insoluble, although CoO is slightly
more soluble than NiO. As will be discussed later, the toxicity of
inhaled particles to cilia and alveolar rnacrophages may help explain
differences in their clearance from the lungs.
5.1.2.2 Metabolism and Excretion
The physiological effects of nickel exposure ultimately depend on
the concentrations of nickel achieved at the cellular and subcellular
-------
level. The physicochemical form of the nickel determines the distribu-
tion within the body and subsequently the relative intracellular con-
centrations achieved.
Several studies have been done on rats of the distribution and
elimination of nickel carbonyl (Ni(CO)4) following an LDjQ dosage
either by the intravenous (22 mg Ni/kg) or inhalation (0.20 mg Ni/liter
of air for 15 minutes) route (Sunderman and Selin 1969, Sunderman at al.
1968, Kasprzak and Sundertnan 1969). The nickel carbonyl was radioactively
labeled either at the carbon (14C) or nickel (63Ni) moiety.
An important finding of these studies was that Ni(CO>4 was rapidly
absorbed by the inhalation route, with levels of nickel carbonyl in
the blood similar to those following intravenous administration. Gas
chromatographic analysis identified Ni(CC»4 as a blood species. Excre-
tion of Ni(CO)4 into expired air and elimination of NiCCO)^ from the
blood were apparently monoexponential and estimates of the half-life
in each case (0.6 hour for excretion and 1.6 hours for elimination) are
in rough agreement, considering the imprecision of the chemical analyses.
In contrast, the elimination of total nickel from the blood had a much
longer half-life, 15 to 20 hours. This is interpreted to mean that
nickel, once disassociated from carbonyl, is removed much more slowly
from the blood. Carbon mcnoxide was released by the decomposition
of ^i(CO)^ within the body, became reversibly bound to hemoglobin, and
was excreted primarily in expired air. Approximately 38% of the intra-
venous dose of Ni(CO)^ was excreted unchanged as Ni(CO)4 in the expired
air, 31% was excreted in the urine, (presumably as Mi"1"1"), and an almost
insignificant fraction was excreted in the feces. The tissue distri-
bution data are imprecise, but indicate a wide distribution of nickel,
including to the brain and spinal column. This is interpreted to mean
that Ni(CO)4 is a "carrier" for nickel. The findings that Ni(CO)4 was
an identified species in che blood and that nickel label was found in
the brain suggest that Ni(CO)4 readily crosses biological membranes.
A study by Oskarson and Tjalve (1979a and 1979b) in which mice were
administered approximately the same dose of Ni(CO)^ (4.5 mg/Ni/kg) by
either intravenous or inhalation routes also indicated that Ni(CO)4 was
decomposed in. vivo and that most of the nickel existed in tissue in the
cationic state (Ni^) . After inhalation, the highest levels of radio-
activity (63\ji) were measured in the lung, brain and spinal column, and
heart muscle at 1 hour. At 1 day an extraordinarily different relative
tissue distribution was seen between intravenously dosed animals and those
which were dosed by inhalation. In particular, there was a much higher
level in the brain in the inhalation-dosed mice. The authors suggest that
the co-administration of ethanol (as vehicle) in the intravenously dosed
mice may have altered the oxidation of- Ni° .
In contrast to the tissue distribution of nickel carbonyl, paren-
teral administration of Mi"1"*" leads to highest tissue levels in the
kidney, endocrine glands, lung, and liver and very little in the
central nervous system (NAS 1975). Organ distribution data do not
5-6
-------
ordinarily reveal the relative intracellular /extracellular distribution.
A suggestion of a low incracellular penetration upon absorption or
parenteral injection is made by kinetic analysis by Onkelinx et al.
(1973). These researchers injected intravenously moderately small
amounts of 63XiCl2 into rats (82 ug Ni/kg) and rabbits (240 ug Ni/kg)
and measured plasma concentration decline, urinary excretion, and
fecal or biliary excretion. A two-compartment open system phanna-
cokinetic model was fitted to the data. (For discussion of the two
compartment model see Greenblatt and Kock-Weser 1975.) Values of some of
the important pharmacokinetic parameters normalized to a per-kilogram
basis for comparison between the two species are listed in Table 5-1.
Nomenclature is somewhat altered to correspond to that used in the
discussion by Greenblatt and Kock-Weser.
This analysis indicates that the central compartment volume
is much larger than the vascular volume (-\,4Q ml/kg) but is close
to the volume of extracellular water (^200 ml /kg) . Also the
peripheral compartment is quite small. The total volume of distribu-
tion (V^ -r VT) is considerably less than the 600 ml/kg total body
water. It sfiould be pointed out that the computed volumes do not
necessarily correspond to volumes of anatomical compartments; however,
it can be tentatively concluded that nickel ion distributes primarily
into extracellular water, and that it does not readily penetrate cell
membranes and, therefore, would not readily cross the blood-brain
barrier.
Excretion of S1++ was found to be primarily via the kidney, which
accounted for "->80% of excretion. Fecal or biliary excretion accounted
for about 10%. Although combined urinary and fecal excretion from the
central compartment was quite rapid (k of 0.1 corresponds to a half-
life of 6.9 hours), the overall rate of elimination from the body
was apparently reduced by the relatively slow equilibration between
compartment 1 and compartment 2, such that the elimination half-life
during the 3 phase was on the order of several days. It should be
kept in mind that the values of these parameters in humans may be
somewhat different (Onkelinx et al. 1973) .
An extensive discussion of the binding of N±++ to plasma proteins
and smaller molecules (e.g., araino acids) can be found in the NAS
monograph (1975). Serum albumin is the principal carrier protein.
Additionally, there exist proteins with higher affinity than albumin
for nickel — so-called nickeloplasmin. The total serum nickel levels
have been found to be remarkably similar among mammalian species, in the
range of 1 ug/1 to 8 ug/1 and somewhat higher in the rabbit (U.S. EPA
1979).
Several studies indicate that serum nickel levels and urinary
excretion reflect recent exposure to nickel. These studies are reviewed
in the N'AS monograph (1975) and the EPA criterion document (U.S. EPA
1979). These reports demonstrate that average plasma concentrations
for workers in a nickel refinery were greater than for non-exposed
-------
TABLE 5-1. PARAMETERS OF THE T/.TO COMPARTMENT MODEL
OF 63Ni(ri) METABOLISM
Source: Based on Onkelinx et al. 1973.
Rat Rabbit
Volume of Central Compartment (ral/kg) 360 205
Volume of Peripheral Compartment Call/kg) 40 78
Percent Excreted in Urine 78 78
Percent Excreted in Feces (bile) 15 (9)
Clearance (tal/kg/hr) 39 18
k£, Total Elimination Rate Constant (hr"1) 0.108 0.088
Ku, Urinary Elimination Rate Constant (hr"1) 0.085 0.078
t 1/2, 2 Phase (hrs) ^9 83
5-8
-------
workers. Exposure to soluble salts of nickel or to insoluble compounds
resulted in increased serum nickel levels. Spruit and Bongaarcs (1977)
found that serun levels of eight occupationally exposed workers averaged
between 1.0 ug/dl to 1.1 ug/dl (10 ug/1 to 11 ug/1) at different periods
of the year, but averaged 0.53 y g/dl (5.3 ug/1) after a two week holiday,
Controls showed plasma levels of 1.6 ug/1 and 2.0 ug/1 in males and
females, respectively.
Urine nickel levels appear to be more difficult to correlate with
exposure due, in part, to the difficulty of obtaining 24-hour urine
specimens and avoiding inadvertent contamination. Calculation of
nickel concentration relative to creatinine to control for renal
function has not usually been done. Bernacki at al. (1978) analyzed
both serun and urine levels of nickel in workers from 12 different
occupational groups. Urine levels and serum levels generally correlated.
The highest urine levels were found on average (+S.D) in nickel refinery
workers (12-t j-_ 109 ug/g creatinine), nickel platers (19 + 15), metal
sprayers (16 ^ 22) f and nickel battery workers (10 *_ 6.4). This com-
pared with levels in non-exposed industrial workers of 2.7 + 1.7.
Individual air concentration sampling in 65 occupationally exposed
workers was carried out over an eight-hour workshift. No significant
correlations between the estimate of the subject's atmospheric exposure
and the concentration of nickel in his urine were observed for any of
the 7 occupationally exposed groups. However, the highest atmospheric
levels (0.489 + 0.560 mg/m3) were determined for the nickel-refinery
workers who also had the highest average urinary levels (124 +_ 109 Ug/g
creatinine).
McMeely et al. (1972) conducted a study of two comparable groups of
healthy hospital employees who had no occupational exposure to nickel.
One population was from Hartford, Connecticut, and the other from
Sudbury, Ontario. Table 5-2 presents the results of this study. On
average 'urinary nickel excretion was higher in the Sudbury group which
had higher nickel exposure from both the atmosphere and drinking water.
The authors emphasize, however, that there was no evidence that the
environmental exposures to nickel in Sudbury were associated with ad-
verse effects in man or animals, or that they were deleterious in any
way to the health of the inhabitants. A comparison of health effects
associated with nickel exposure experienced by inhabitants from differ-
ent locales would be extremely difficult to interpret because of the
numerous socioecononic and other exposure variables to be considered.
5-9
-------
TABLE 5-2. RELATIONSHIP OF NICKEL EXPOSURE TO URINARY
EXCRETION OF NICKEL
Ni in Tap Water Si in Air Urinary Nickel Excretion
Location Cug/1) (yg/lQQO m-^) ug/1.73 m-/dayb yg/g creatinine
Hartford 1.1+0.3* 36 2.4+1.3 2.3+1.3
Suobury 200 + 43 5333 7.5 + 3.3C 5.9 + 2.8C
.lean +_ standard deviation.
Each subject's daily excretion was adjusted for his body surface area.
CP < 0.001 vs. Hartford group.
Source: McNeely et al. (1972)
5-10
-------
5.1.3 Carcinogenicity
5.1.3.1 EpideT.iological Studies
Nickel's role as an occupational carcinogen via inhalation, parti-
cularly in the nickel refining industry, has been given considerable
study. Several recent reviews have detailed the epidemiological findings
(NAs'l975, Sunderman 1973, Sunderman 1976, and IARC 1976).
A number of factors prevent any useful prediction from the epidemio-
logical studies of the risk of respiratory tract cancer due to nickel
exposure. Chiefly, there are no good estimates of the exposure to
nickel of nickel workers in terms of concentrations or speciation.
Concomitant exposure of workers co arsenic, chromium, cobalt, smoking,
asbestos, and polycyclic aromatic hydrocarbons makes uncertain the
primary role of nickel in the etiology of respiratory tract cancer.
The importance of co-exposure variables has been noted in the more
recent literature (see Kreyburg 1978 and Langer et al. 1980 for examples).
Nevertheless, it appears to be the conclusion of most authorities who
have reviewed the problem that nickel is a primary factor in the develop-
ment of respiratory tract cancer in nickel refinery workers. The animal
experimental data, discussed below, support this conclusion.
A careful review of all the epideniological studies would not only
be a prodigious undertaking but also seem destined to equivocation,
particularly if the goal was to provide risk estimates. The inadequacy
of quantative exposure data both for nickel and co-existent toxic com-
pounds precludes evaluation of the dose-response relationship. Two
studies are summarized here to illustrate a few of the problems.
Kreyberg (1978) reached no definitive conclusions concerning the
relationship between nickel exposure and lung cancer, but discussed
the variables of cigarette smoking, time factors, and the relative
incidences of lung-tumor types among different occupational groups.
Smoking was prevalent among cases of lung cancer in nickel-refinery
workers; 32/39 cases were smokers. Kreyberg identified a long latency,
in the range of 16 to 40 years, between first exposure to nickel and •
diagnosis of lung cancer. The importance of the smoking factor suggested
that the latency between the start of smoking and diagnosis of cancer
could be more relevant; moreover, there could be an age-dependent sus-
ceptibility to lung cancer that would partly determine the age of diag-
nosis. The number of cases of lung cancer roughly correlated with the
number of people employed in the Falconbridge Nickel Refinery and with
the availability of cigarettes. During World War II, production and
the number of men employed dropped and cigarettes were a scarce commodity.
5-li
-------
A previous study by Xreyberg had found an association between increased
smoking and the incidence of lung cancer in Norway. Krevberg stated
that the true risk to a healthy person of developing lung cancer as a
nickel worker could only be measured in a population of non-smokers.
It is suggested, however, that a scudy of non-smokers nay be impractical
and would leave unanswered the more important question concerning inter-
action of smoking and nickel exposure.
Nickel carcinogenesis following ingestion does not appear to be an
area for concern. This conclusion is based on the poor gastrointestinal
absorption of nickel, the efficient mechanisms of excretion, and the
results of animal studies which indicate that high dietary levels of
nickel are without measurable carcinogenic effects.
5.1.3.2 Aninal Studies
Table 5-3 summarizes the data on the carcinogenicity of nickel
carbonyl. The usual route of exposure to nickel carbonyl is by inhala-
tion. The studies of Sunderman and coworkers (1965, 1959, and 1957)
suggest that nickel carbonyl is carcinogenic by the inhalation route,
although there was a very poor survival rate of test animals. Kincaid
et gl_._ (1953) reported that rats who survived for 1 to 2 days after
exposure to LC5Q levels of nickel carbonyl (0.2 mg/1 for 30 minutes)
showed extensive pneumonitis. Those that died within several hours
showed severe pulmonary congestion and edena. Histological sections
showed intestial pneumcnitis, areas of atelectasis, and other areas
with necrosis. Large amounts of brown-black pigment were present
throughout the capillaries of the alveolar walls. The acute toxicity
to the lungs of nickel carbonyl has been found to be similar in experi-
mental animals and man (see Section 5.1.4,3).
In a study by Lau et_ al . (1972) , intravenous injection of a total
of 158 mg nickel carbonyl/kg ^n divided doses caused a significant number
of malignant tumors throughout the body over the lifetime of the rats.
Intravenous injection of nickel carbonyl is comparable to inhalation
because the compound rapidly distributes via the blood to all tissues
when dosed by inhalation exposure. Furthermore, much of the nickel
carbonyl is excreted unchanged via the lungs after either intravenous
or inhalation exposure.
Survival of test rats in this study was comparable to that of
untreated rats and all rats were allowed to die of "natural" causes
or were killed when moribund. This study is considered adequate for
risk extrapolation for nickel carbonyl.
Ottolenghi and coworkers (1974) exposed rats by inhalation to
(for details on exposure see Table 5-4) , and reported highly significant
lung pathology, including 14% lung neoplasms versus 1% in unexposed rats.
This study is considered adequate for risk extrapolation in terms of
duration, survival of test animals, number of animals tested, and the
5-12
-------
TAIJI.K 5-3. CAUCTNOCKNICTTY STUD IKS WITH N'ICKKL CAKI5ONYJ, (Ni(CO)z,)
An i ma I
Wistar Kat
Koute/Dosage
Inhalation: 0.03 mg/1 for 30
min, 3 times per
week for 12 months
0.6 mg/1 for 30 min,
single exposure
0.6 mg/1 for 30 min,
single exposure treated
with Dlthiocarb
Uistar Kat
Sprague-
DawJey Hat
Inhalation: 0.03 mg/1 for 30 min,
3 times per week for
12 months
0.06 mg/1 as above
0.25 mg/I for 30 min,
single exposure
Intravenous: 20 pi/kg
(9 mg Ni/kg) 6 doses
Response
[Control ()at/»_{_ Ri'fi'
1/8 rats surviving ^ 2 yrs had Sunderman and Donnelly
pulmonary carcinoma with metastases. (1963)
1/35 rats surviving 2 yrs had pul-
monary adenocarcinoma with metastases.
1/27 rats surviving 2 yrs had anaplastic
lung carcinoma
[0/44 rats surviving at least 2 yrs had
pulmonary carcinoma]
1/5 rats surviving > 2 yrs had neoplasms Suiulerman et al.(1957)
of the lung Sunderman et "a I. (1959)
1/1 rat surviving > 2 yrs had neoplasms
of the lung
1/3 rat surviving > 2 yrs had neoplasms
of the lung
5/121 rats had pulmonary lymphomas Lau et al. (1972)
14/121 rats had additional malignant tumors " ~~
at intervals of 2-4 wks. at varied sites
50 pi/kg (22 mg Ni/kg),
single dose
6/72 rats had malignant tumors at varied
sites
[2/47 rats had pulmonary lymphomas]
[0/47 rats had tumors at additional
sites]
-------
TABI.K 5-4. CARCINOCKNICITY STUDT.liS WITH NICKMI. SUB.SUI.n DK (NJ3,S;>)
Animal
Wistar Rat
Fischer 'J44
Rat
Ul
I
Route/Dos age
Response
Jntratr.-ieheal: 5 ing/animal
mean particle diameter 10 jim
Inhalation: 1 mg/m
6 hr/day, 5 days/week for
78 weeks
Particle sizes:
70% < 1 Min
1 urn < 25% < 1.5 inn
Reference
0/13 rats had pulmonary tumors in 15 months Knspr/.ak i-t al. (197 i)
4/13 rats liad peribrondiial adenomatoid
proliferation
[No controls]
Preneoplastic and Neoplastlc Lung Lesions(%) Ottolc-nglii et al. (1974
Atypical Hyper-
plasia
Squamous meta-
plasia
Lung neoplasms
Control
28 (13)
10 (5)
2 (1)
Test
106 (51)a
38 (I8)a
29 (I4)a
Other neoplastic findings: 12%a incidence of adrenal
medullary nodular hyperplasia and pheochromocytomas
in test animals compared to 1% in control.
Other Lung PatholoRy(%)
Pneumonitis (14)
Atelectasis (5)
Bronchitis (5)
Bronchiectasis (3)
Rmphysema (6)
(48)a
(16)a
(12)a
(12)a
0.01
0.05
-------
thoroughness of post-mortem examination. Both males and females were
tested, and there were no marked differences between the saxes in the
response to the ti^S^ exposure. This study is used as a basis for
predicting risk of lung neoplasms in humans exposed to
Elemental nickel and NiO have not been shown to be carcinogenic by
the inhalation or intratracheal routes (Tables 5-5 and 5-6) . In com-
parison to nickel carbonyl and nickel subsulfide, these nickel compounds
caused less severe adverse pulmonary reactions. Further discussion of
pulmonary toxicity appears in Section 5.1.3.1.
5.1.3.3 Carcinogenicity Studies Using Other Routes of Administration
As has already been discussed, nickel salts are poorly absorbed
via the oral route. There has been no demonstration of carcinogenic
activity by the oral route in humans or in animals (NAS 1975, U.S.
EPA 19 79 ) . '
Numerous investigators have administered intramuscular, subcutaneous,
or intraperitoneal injections of nickel and nickel compounds to induce
local sarcomas as a preliminary step in studying morphology, biochemistry,
and the effects of cheraotherapeutic regimens in cancer. Sunderraan (1976)
remarked that N13S2 carcinogenesis is an attractive experimental model
because the compound is inexpensively available in high purity and is
readily labeled with 63Ni, which is ideally suited for liquid scintil-
lation spectrometry and auto-radiography.
However, injection-site tumors from nickel compounds are probably
not relevant to the risk assessment. On the one hand, the IARC working
group (IARC 1976) has pointed out that injection-site tumors require
careful consideration because of the possibility of non-specific action
of the vehicle or the physical effect of the agent. Injections of
finely divided forms of nickel compounds are not comparable to the
exposure of human populations. It has been noted that carcinogenicity
following subcutaneous injections is inversely related to solubility of
the injected nickel compound. Clearly, one of the reasons for this
is that soluble salts do not remain at the injection site, but are
carried away and rapidly excreted.
On the other hand, the insoluble nickel compounds have been demon-
strated to be slightly soluble in in vivo and in vitro experiments.
Nickel ion is conplexed with many large (proteins) and small (e.g.,
amino acids) molecules so that transport across cellular membranes
(by phagocytosis, pinocytosis, facilitated transport) does occur.
Intracellular Ni ion affects metabolism and in particular becomes
closely associated with nuclear elements (Sunderman 1976). Nickel is
one of the metals in the stainless steel alloys used in implant materials
such as for bone fixation, joint replacement, and heart valves. The
reports of two cases of tumors in humans at the sites of stainless
steel implants (NAS 1975) and allergic sensitivitv reactions to stain-
less steel implants that resolved after the implants were removed (U.S.
5-15
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TAm.li 5-5. CAUCINOCKNI CITY STUDIKS WITH KUiMKNTAI. NICKKL
Animal
Mouse
Inhalation:
Route/Dosage
Ke spouse
15 mg/m , 6 hr/clay, 4-5
clays/week until death,
99% pure - particle
diameter < 4 |im
Hat
Guinea Pig
Same
Ul
i
No abnormalities of bronchial
mil cos a
15/50 rats and most guinea pigs
showed abnormal multicentric
adenomatoid formation affecting
alveolar structures and atypical
proliferations of the epithelial
lining of the terminal bronchioli ,
Rats showed inflammatory changes
and nuicosal ulcers in the para
nasal sinuses. ]. group showed ana-
plastic Jntraalveolar carcinoma,
extensive adenomatosis, and a
possible metastasis from lung in
the abdominal cavity.
[Control: the adenomatosis seen in
the test group of guinea pigs was
noted in 5/9 controls but was not
diffuse as In test animals. Gener-
ally, there are inadequate control
data].
Reference
llueper (1958)
Rat
Hamster
Inhalation: level unspecified
99% pure - plus 20-35
ing/kg (sic) S02 and pow-
dered limestone I part to
3-4 parts Ni (to prevent
conglomerates)
0/46 tumors in rats surviving > 18
months
0/66 tumors in hamsters surviving
> 18 months
Hueper and Payne (1962)
-------
TABLE 5-6. CAIUMNOCI'N ICITY STUIHKS WITH NTCKKL OX 11)1- (Ni(>)
An I ina
Reference
Hamster
4 mg/animal once a week for 30
weeks by Jntratracheal injection.
Particle diameter: 0.5-1.0 urn
Controls received nut-shell
charcoal Ln place of NiO
1/50 tumor of respiratory tract
in test animals.
4/50 tumors of respiratory tract.
Tarrej I and Davis (l'J74)
Syrian Ho 1 den
Hamster
Ul
I
inhalation: 52 pg/l, 7 hrs/day
5 days/week for 1ifuspan.
Particle diameter: 0.3 Mm
4/51 malignant tumors at various
sites.
1/51 controls.
Authors concluded no carcino-
genic effect due to NiO.
Wehner el al. ( llJ75a)
(19751)) ( iy"7'J,-i)
Asbestos fiber inhalation
23
10/102 lung adenomas
-------
EPA 1979) suggest chat the alloys are not totally inert. The cases
of tumors at implant sites in humans are anecdotal. Comparisons of
these complications and those with other implant materials and appropri-
ately controlled studies would have to be carried out to assess whether
or not tumorigenesis associated with internal protheses is a significant
health problem.
The injection-site turaorigenesis of nickel in experimental animals
has been extensively reviewed elsewhere (NAS 1975, U.S. EPA 1979, Sunder-
man 1973, and Sunderman 1976).
5.1.3.4 Mechanisms of Nickel Carcinogens
Various lines of research have been pursued to determine the mech-
anisms of nickel carcinogenesis. An essential first step is penetration
of the cell membranes by the nickel compounds. As discussed above,
nickel carbonyi can diffuse across biological membranes because of its
lipid solubility and relative stability in vivo. It decomposes,
liberating Ni" which is then oxidized to Ni^"! Ni++ has been shown
to react with a variety of intracellular constituents. Nickelocene is
also lipophilic and, therefore, would be expected to penetrate biological
membranes by diffusion.
Singh and Oilman (1973), using a double-diffusion chamber implanted
intraperitoneally in rats, demonstrated that nickel subsulfide had a
sufficient solubility in vivo to diffuse across a filter of pore size
0.1 urn and to disrupt the normal growth of embryonic rat skeletal
muscle in the adjacent chamber.
Webb and coworkers have shown that metallic nickel powder gradually
dissolved when incubated with horse serum or muscle homogenates and
that the nickel is complexed with serum proteins and ultrafilterable
molecules (Heath _et _al. 1969, Weinzierl and Webb 1972). Webb and
Weinzierl (1972), using cultured C57S/1P mouse dermal fibroblasts, studied
the cellular uptake from media containing 63Ni'H' complexes and the re-
lative intracellular distribution of °%i. The concentration in the
culture media was 7-10 ug/tnl of Ni++ complexes. After 48 hours, approxi-
mately 3.5% of 63^i was bound to the cell monolayer and 97% of this was
released when trypsinization of the monolayer was performed to separate
cells and isolate them. The nickel content in the isolated cells was
0.023 ug 63Ni or 0.04% of the nickel available from the media. The
approximate intracellular distribution determined after fractionation
was nuclear fraction, 37%; cell sap fraction, 30%; mitochondrial fraction,
23%; and microsomal fraction, 11%. Of the nuclear fraction, 50% was
isolated with the nucleoli and 20% with the nuclear sap. The authors
do point out, however, that the quantitative measurements of intra-
cellular distribution are subject to certain limitation because losses
and transfers between fractions may occur during cell isolation and
the f ractionation procedure. While intracellular uptake of Ni"*"^ is
indicated, it is clearly extremely lew.
5-18
-------
Phagocytosis of insoluble nickel compounds by alveolar macrophages
(Johansson and Caraner 1980) and by Syrian hamster embryo cells and
Chinese hamster ovary cells (Costa and Mcilerihauer 1980) demonstrates
another means of intracellular transport. Once within the cell enclosed
in vacuoles, the particles are subjected to catalytic enzymes and altered
pH which could ultimately release nickel intracellularly. Johansson
and Camner (1980) proposed that alveolar macrophages may transport
nickel to lymph nodes. These researchers exposed rabbits for 3 months
(5 days/week, 6 hours/day) to metallic nickel dust (1.2 mg/m-') and
reported finding nickel particles within macrophages from the hilar
lymph nodes. They concluded that the macrophages containing nickel
particles passed across the alveolar wall and then to the nodes. They
also concluded that the nickel particles did not cross the alveolar
walls to be subsequently taken up by macrophages because of morphological
similarities of the "laminated bodies" found in both the alveolar and
lymph node macrophages.
Sunderman and coworkers have studied the intracellular mechanisms
of Mi toxicity. In the initial study (1967a) on this aspect of Ni
toxicity, Sunderman found that "i(CO)4 administered to rats at LD5Q
dosage by either intravenous injection (22 ng Mi/kg) or inhalation
(0.2 mg Ni/1 air for 15 minutes) inhibited phenothiazine induction
of hepatic cell benzpyrene hydroxylase activity. Maximum inhibition
occurred when Si(CO)4 was administered approximately 24 hours before
induction. In vitro benzpyrene hydroxylase activity was not inhibited
by added Ni"H-. That benzpyrene hydroxylase synthesis was probably
inhibited was indicated in a second study (1967b). Nickel carbonyl
(LD5Q dose, IV) inhibited cortisone induction of hepatic tryptophan
pyrrolase activity; however, the enzyme activity was not significantly
different between control and test [Si(CO)4 pretreatment of rats] pre-
parations when tryptophan was administered to increase the enzyme levels.
Tryptophan increases hepatic tryptophan pyrrolase activity by decreasing
the enzyme's catalysis, while cortisone increases synthesis of messenger
RXA template for enzyme production.
Further evidence that Ni inhibited synthesis of heptatic enzymes
was reported by Sunderman in 1968. In this experiment the effect of
nickel carbonyl (LD5Q dose) on induction of hepatic cytochrome P-450
activity was studied. The enzyme was measured spectrophotometrically
so that changes in levels of important co-factors in enzyme reactions
could be discounted as a cause of the ability of Si-1-*- to block induction
of hepatic enzyme activity. Ni(CO)4 inhibited the induction of the
enzyme, not the enzyme's in vitro activity. In this case, there was
a definite reduction in tissue concentration of the cytochrome P-450
from Si(CO)4-treated rats compared to the concentration in control
tissue.
Beach and Sundeman (1970) further clarified the site of action
of nickel carbonyl by demonstrating that administration of the compound
to rats inhibited R^A synthesis by the chromatin-RNA polymerase complex
prepared from lysed hepatic nuclei. Thus, inhibition due to impaired
5-19
-------
transport of RNA precursors across Che nuclear membrane was apparently
ruled out. Control chromatin-RNA polymerase complex was not inhibited
whan treated in vitro with Ni(CO)4 or Ni Cl2 at concentrations 3 times
higher than the Ni concentration remaining in the in vivo treatment
preparation. This result suggested that Ni"1""1" does not interfere with
RNA synthesis directly but at some earlier step, perhaps at the DNA
level.
The effects demonstrated by Sunderman and coworkers do not neces-
sarily represent carcinogenic mechanisms but may be relatively non-
specific toxic responses of physiologically damaged cells. The high
toxic dose of nickel carbonyl should be expected to have a multitude
of effects at the biochemical level, many of then indirect and non-
specific. The penetration to and disruption of nuclear processes by
nickel may be secondary to cellular damage because the cell cannot
maintain the normal membrane barriers and intracellular milieu. An
inference that these studies may illustrate a co-carcinogenic role of
nickel (as nickel carbonyl) is also probably unwarranted because the
doses were extremely high.
5.1.3.5 In Vitro Assays of Carcinogens
DiPaolo and Casto (1979) studied inorganic metal salts in a trans-
formation assay using Syrian hamster embryo cells (EEC). Salts of
nickel, cadmium, chromium, beryllium, and arsenic were positive
(induced transformation of cells) in this assay, but salts of iron,
titanium, tungstate, zinc, aluminum, and amorphous nickel sulfide
(XiS) were negative. With the exception of the results for cadmium,
these results generally correlate with those from animal and/or human
studies of carcinogenicity. In a later study (Costa et al. 1979),
undifferentiated sarcomas developed in 26 of 27 nude mice at the site
of subcutaneous injection of clones of Ni2S3-transformed cells, and
no tumors developed in 19 control nude mice given subcutaneous injections
of control, non-trans formed Syrian hamster embryo cells. Costa and
Mollenhauer (1980) determined that amorphous NiS was not phagocytized
by Syrian hamster embryo cells or by Chinese hamster ovary cells but
Mi3S2 was actively phagocytized. These authors suggest that carcinogen-
icity may be dependent on cellular uptake.
Nishiraura and Umeda (1979) and Umeda and Nishimura (1979) studied
the ability of metal compounds to induce chromosome aberrations in
FM3A cells frcn C3H mouse mammary carcinoma. Compared with chromium
(-T-6 valency) compounds, Ni compounds were poor inducers of chromosome
aberrations. Aberrations, principally gaps, were greater than in con-
trol cultures at concentrations between 2 and 10 x 10~^*M. Twenty x
10~^M was lethal to the cultures. The ability of Ni compounds to
induce chromosome aberrations became somewhat more apparent when cells
were first treated in various Ni media (6 to 10 x 10~^M) for 24 or 48
hours and then incubated in control medium. During recovery, the percent-
age of aberrant chromosomes, again principally gaps, tended to reach a
maximum after 24 or 48 hours and fall off to control levels after 1
5-20
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or mora days. Taking the overall incidence presented by Nishimura and
I'neda, the nickel compounds appear Co induce low levels of chromosomal
aberrations at concentrations that are also toxic to the cells. It
should be noted that the aberrations induced are mostly, if not exclus-
ively, gaps which are not scored as chromosomal aberrations by sone
investigators because of the subjective nature of scoring gaps.
5.1.4 Other lexicological Effects
5.1.4.1 Chronic Inhalation Toxicity
Low-level chronic inhalation toxicity to nickel compounds has not
been studied in man or animals adequately to make estimates of levels
of exposure which cause no effects. A brief report by Torjussen and
Solberg (1976) on a pilot study stated that of 92 nickel-exposed workers,
17% were found to have had atypical epithelial changes in nasal biopsy
specimens from the niucosa of the middle turbinate. No such changes
were found in the 37 controls who had no known exposure to nickel.
Exposure levels and a description of the study population were not
given in this report. 3oth carcinogenic response and non-carcinogenic
lung pathology have been summarized in Tables 5-3 through 5-6. The
results for ^1382 inhalation in rats (Ottolenghi and coworkers 1974)
are particularly alarming.
'.•"ehner and coworkers (Wehner and Craig 1972, Wehner e_t_ a_l_._ 1975a,
Wehner et al. 1975b, Wehner e^ al. I979a, Wehner ejt_ al^ 1979b) have
studied the inhalation toxicity of NiO, CoO, and chrysotile asbestos.
Differences in the clearance of NiO and CoO from the lungs were
found. Histopathological evaluation of lung sections frora chron-
ically exposed hamsters (53 mg NiO/raJ, 7 hours/day, 5 days/week) indi-
cated accumulation of NiO within the alveoli. After short periods of
exposure (unspecified by the authors but presumed to be on the order
of months), there was little cellular response. After longer periods
of exposure, the nature of the cellular response was both inflammatory
(macrophage accumulation containing phagocytized NiO particles) and
oroliferative ("alveolar septal cell hyper-plasia," "epithelial pro-
liferations from bronchioles, and bronchiolization of alveoli").
Pneuraoconiosis was more pronounced in the NiO-axposed animals than
the CoO-exposed animals. Pneuraoconiosis was defined to "include
interstitial pneumonitis and diffuse granulomatous pneumonia which
were frequently more severe in focal areas, fibrosis of alveolar septa,
bronchial and bronchiolar (basal cell) hyperplasia, bronchiolization of
alveolar epithelium, squamous metaplasia, and emphysema and/or atelectasis
of varying degree." There was no clearer breakdown relating duration
of exposure to incidence of specific respiratory tract lesions.
Wehner and coworkers found no malignant tumors or premalignant
lesions of the respiratory tract in hamsters exposed to NiO for their
5-21
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entire lifetime (53 mg/1, 7 hours/day, 5 days/week). In 102 asbestos-
exposed banisters, 10 lung adenonas were seen. These lesions are con-
sidered to be preir.alignant. Two other lung adenomas were apparently
seen but in which groups they occurred could not be determined from the
investigators' reporting.
Since alveolar macrophages are considered an important defense
mechanism against inhaled substances such as bacteria, reports of the
toxicity of respirable metal dusts to alveolar macrophages are of some
interest. It is unclear, however, what indexes of toxicity are appro-
priate and what levels of toxic response can be considered as deleterious
to humans.
Graham and coworkers (1975) measured the viability and phagocytic
activity of alveolar macrophage (obtained from untreated rabbits). The
alveolar macrophages were treated in vitro with 703, Mi++, Cd-H-, Cr'H~!',
and Mn"^. Ni^ markedly decreased phagocytic activity of alveolar
nacrophages at concentrations (e.g., 0.8 mM) that were only slightly
cytotoxic, while V03~ was cytotoxic at concentrations (e.g., 0.7mM)
that did not affect phagocytic activity of the remaining viable macro-
phages. With Cd2+, Cr^-r, and Mm2+j viability and phagocytic activity
were decreased more in parallel.
In contrast to Graham's results, Camner et al. (1978) measured an
apparent increased phagocytic activity (uptake of silver-coated Teflon
particles in vitro) of alveolar macrophages obtained from rabbits
exposed to metallic Ni dust (0.5 or 2.0 mg/m^ for 4 weeks, 6 hours/
day, 5 days/week) when compared with macrophages from non-exposed
rabbits.
Aranyi _et _al. (1979) studied the effects of coal fly ash (FA)
coated with PbO, NiO, or Mn02 on alveolar macrophages obtained from
untreated rabbits. The order of toxicity based on viability, total
protein content, or lactic dehydrogenase activity was PbO/FA > NiO/FA >
Mn02/FA > untreated FA. Decreased viability appeared to be the most
sensitive indication of toxicity.
Another defense mechanism of the lung is inuco-ciliary clearance.
Adalis and coworkers (1978) reported that Ni at concentrations of 0.011
mM decreased ciliary beating frequency in an in vitro model using
isolated hamster tracheal rings. Exposure of hamsters to MiCl2 aerosol
at concentrations of 100 to 275 vig of nickel/m^ (2 hours/day for 1 or
2 days) also decreased ciliary beating frequency as determined in vitro.
The tracheal rings were removed from the treated animals 0, 1, 2, or
3 days after the exposure for the in vitro tests. The beating frequency
was depressed at all times compared to control.
One of the possible consequences of these effects was indicated in
studies by Port and coworkers (1975) and Adkins and coworkers (1979).
Port reported that XiO (intratracheal instillation of 1-5 mg, <5 urn
5-22
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diar.eter) significantly increased mortality from an influenza virus in
hamsters. Mortality was highest when I'iO was administered 24 hours before
the influenza virus exposure (routa not indicated). Pathological changes
in che lung were exacerbated when the sequence of influenza NiO exposure
was reversed. Adkins reported increased mortality due to inhaled strep-
tococci in mice pretreated with a 2-hour exposure to nickel chloride
aerosol (499 ug Ni/m^). He also reported a significant reduction in
phagocytic activity of alveolar oiacrophages obtained 24 hours after
nickel chloride exposure.
5.1.4.2 Reproductive Effects
The erabryotoxicity and teratogenicity of nickel carbonyl were
reported in abstract form by Sunderman and coworkers (1978a). Pregnant
rats were exposed on day 8 of gestation to Ni(CO)4 by inhalation in
dosages of 0.06 mg/1 or 0.12 mg/1 air for 15 minutes. These two dosages
correspond to approximately l/10th and l/5th the LDso dosage. Table
5-7 indicates significant erabryotoxic and teratogenic effects of nickel
carbonyl.
In another study, Sunderman and coworkers (1978b) found no terato-
genic effects of either nickel chloride (16 mg/kg) or nickel subsulfide
(80 mg/kg) in rats. Dams were injected intramuscularly on Day 6 or 8
of gestation. Results showed that nickel ion did cross the feto-maternal
barrier. The effects that were seen were a reduced number of pups per
dam and diminished body weights of the fetuses and weanlings 4 to 8 weeks
after birth.
Feeding studies have tended to show adverse effects of nickel salts
on reproduction. Schroeder and Mitchener (1971) followed three generations
of rats continuously exposed to nickel (as Ni++) in drinking water at
5 mg/1. This level corresponds to approximately 0.4 mg/kg/day (5 mg/1 x
0.025 liters/day T 0.3 kg b.w.). Increased numbers of runts and increased
neonatal mortality were seen in each generation. Moreover, there were
significant reductions in litter size and a reduced male/female sex ratio
in the third generation.
Ambrose and coworkers (1976) followed three generations of rats
given nickel in their diet at 250-1000 mg/kg. Assuming food consumption
is normal at ^ 15 gin/rat, these levels correspond to ^ 4 and 15 ug/rat
or 1750 to 7000 times average human nickel intake. Food consumption
was reduced at the 1000-mg/kg level in all generations and, perhaps
for this reason as well as nickel toxicity, there was increased fetal
mortality in the first generation.
Subcutaneous dosing of 2.4 mg N'i/kg to male rats caused abnormal
histopathology of the testis with disintegration of spermatozoa 18 hours
after a single dose; the effects were reversible (Hoey 1966). Another
study cited by MAS (1975) also demonstrated gametotoxic effects in rats
dosed orally with 25 mg/kg. The male rats were apparently infertile.
Gametotoxic effects have not been documented in humans.
5-23
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TABLE 5-7. E:-SRYOTOXIC AND IHRATCGENIC EFFECTS OF INHALED NICKEL CARBONYL
Dosage, mg/1 x 15 min
Live Fetusas/Dan
Dead Fetuses/Conceptuses
3ody Weight of Live Fetuses
Ophthalmic Malformations
Response to Treatment _(±3D)
0 0.06 0.12
9.2 (±2.1) 7.2 (+3.1) 6.3 (+4.7)a
4/114 2/45 IS/593
3.4(+0.2)g 3.0(+0.4)g 2.8(+0.3)g
0/110 12/43a 12/44a
< .02
Source: Sundernian at al. (1978a)
5-24
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5.1.4.3 Acute Toxicity of Nickel Carbonyl
Nickel carbonyl is probably the nose toxic nickel compound. Because
of this and because of its likely carcinogenic and teratogenic effects,
it requires special consideration. The acute toxicity is similar in
animals and humans; nickel carbonyl is about 100 times as toxic as carbon
monoxide. Table 5-8 shows that central nervous system effects predominate
initially upon acute exposure.
As has been indicated in animal studies, there is rapid distribution
of nickel carbonyl to all tissues,roughly in proportion to blood supply,
and ready passage across cell membranes. Excretion via lungs is an
important means of elimination. Intracellularly nickel carbonyl breaks
down to Nie and CO. CO is subsequently handled as in carbon monoxide
poisoning; it binds hemoglobin competitively displacing oxygen carrying
capacity and is slowly excreted primarily as CO in exhaled gases. Ni°
is oxidized to Ni(II) and much of it becomes bound to serum proteins.
Serum Ni(II) is rapidly cleared via the kidney.
Due to the rapid and extensive distribution in the body of nickel
carbonyl, most tissues are affected but the lung is the primary target
organ. Kincaid and coworkers (1953) reported that after a 30-minute
inhalation exposure in rats to 0.24 mg/1, pulmonary congestion and edema
were apparent at one hour. Twelve hours to 6 days later lung histopathology
was reported as interstitial pneumonitis with focal atelectasis and
necrosis. Focal necrosis was apparent in other major organs. The
pathologic lesions of the lung in human exposure are very similar (NAS
1975).
Recovery from nickel carbonyl poisoning is slow, requiring several
weeks. Prompt administration of chelating agents, most notably sodium
diethyldithiocarbamate, significantly reduces the severity of toxicity
and is indeed life-saving.
5.1.4.4 Nickel Dermatitis
Nickel allergy has been recognized as an occupational problem where
workers are exposed to nickel and its salts, particularly in nickel
mining and refining. Other sources of occupational exposure include
manufacture or use of nickel-cadmium batteries, nickel catalysts, ceramics,
duplicating machines, certain dyes and inks, electronics, electroplating,
jewelry making, rubber, and spark plug manufacturing (NAS 1975). According
to the NAS report, occupational exposure is less of a problem today than
in the past due to improvements in protecting workers from exposure, but
non-occupational exposure, principally through skin contact, is very
widespread. Sources include jewelry, coinage, clothing fasteners, tools,
cooking utensils, stainless steel kitchens, detergents, prostheses and
other medical appliances, and tobacco smoke.
The seriousness of the problem in the non-occupational setting is
difficult to evaluate in terns of pair, and suffering, but probably is
-------
TABLE 5-8
CLINICAL MANIFESTATIONS OF NICKEL CARBONYL POISONING IN 25 MEN
,a
Immediate symptoris
Latent period
Delayed symptoms
Physical and x-ray
findings
Laboratory findings
Clinical course
Dyspnea (80%), fatigue (80%), nausea (76%),
vertigo (442), headache (36%), odor of
"soot" in exhaled breath (36%), vomiting
(24%), and insomnia and irritability (24%)
In half of the subjects, an asymptomatic inter-
val between recovery from initial symptoms
and onset of delayed symptoms
Dyspnea with painful inspiration (80%), non-
productive cough (64%), muscular weakness (44%),
substernal pain (44%), chilling sensations
(32%), muscular pain (28%, sweating (24%),
visual disturbances (12%), diarrhea (12%),
abdominal pain (4%), muscle cramps (4%),
and hypoesthesia in legs (4%)
Tachypnea and tachycardia (80%), interstitial
pneumonitis on x-rays (60%), fever (40%), and
cyanosis (36%)
Pulmonary-function tests consistent with
interstitial lung disease (40%), increased
serua glutamic pyruvic transaminase (36%),
increased serurr. glutamic oxaloacetic trans-
amiaase (32%), and low arterial pO_ (32%)
Interval before hospitalizacion.: median, 2 days;
range, 0-7 days. Duration of hospitalization:
median, 6 days; range, 0-27 days. Interval be-
fore recovery: median., 38 days; range, 1-3S
days. Symptoms that persisted for more than
3 weeks: fatigue (S8%), exertional dyspnea
(52%), muscular weakness (48%), headache
(36%), abdominal pain (36%), muscular pain
(32%). sweating (24%), visual disturbances
(16%), and muscle cranps (S«).
Based on observations of Vuopala e_t_ _al_. (1970)
Source: NAS (1975)
5-26
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not directly life-threatening. The incidence of nickel allergic contact
sensitivity has been variously estimated between about 5 and 12% and is
nuch more common in women than in men. Fisher (1967) found that nickel
caused mora instances of dermatitis than all other metals combined.
The chemical pattern of nickel dermatitis begins as itching or burn-
ing (papular erythema); this usually occurs at the sites of contact (sus-
penders, earrings), but often can become far removed from the apparent
area of contact. The eruption usually presents as a papular (raised
bumps) or papulovesicular (bumps with blisters) dermatitis with a ten-
dency for lichenification (thickening of the epidermis). A puzzling
feature of nickel dermatitis is that some cases persist for months after
removal of the apparent offending agent; nickel fixation in the skin and
subtle re-exposure to environmental nickel products have been hypothetized
as reasons for the chronicity (NAS 1975).
5.1.5 Summary
5.1.5.1 Derivation of the Water Quality Criteria
The water quality criteria for nickel were based on the results of
the study by Schroeder and Mitchener (1971) which indicated toxicity to
rats in a three-generation reproduction study (increased neonatal
mortality, increased numbers of runts, and reduced male/female sex
ratio) . Test animals were given nickel in the drinking water at 5 tng/1
which, with nickel in food included, was calculated by the EPA (U.S.
EPA 1980) to be approximately 0.443 mg/kg/day. Using an uncertainty
factor of 1000, the average daily intake (ADI) was computed for a 70-kg
human as 0.031 mg Ni/day. A water concentration of 13-4 rag/1 was cal-
culated that would give this ADI assuming 2 liters of water/day plus
0.0065 kg/day of fish/shellfish products with a bioconcentration factor
47 for nickel.
The EPA (U.S. EPA 1980) states that the average drinking water
levels are 6ug/l; however, nickel in water contributes only about 2-3%
of total nickel ingested because food is the major source of ingestion
of nickel.
5.1.5.2 Additional Health Effects in Risk Assessment
Exposure to nickel salts through ingestion would appear to pose
very little risk because of very low gastrointestinal absorption and the
presence of efficient excretion mechanisms for elimination of nickel
from the body.
The principle routes of exposure to nickel compounds which are
associated with adverse effects are inhalation and skin contact. Nickel
workers who are exposed to a variety of nickel compounds are one of the
special groups at risk. Animal studies indicated that nickel carbonyl
or respirable particulates containing nickel subsulfide were carcinogenic
5-27
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and that ether insoluble nickel compounds caused adverse effects on
the lungs. These data tend to support the view that certain nickel
compounds were causally related to the increase in respiratory tract
cancers in nickel workers. The ability of various insoluble nickel
compounds to cause pneumonitis and atypical cellular changes in the
upper respiratory tract nay suggest a co-carcinogenic role of these
nickel compounds or at least some synergy in the development of lung
diseases.
Nickel carbonyl is an extremely poisonous substance and is probably
carcinogenic.
The other major effect of nickel is dermatitis which has been an
occupational problem in industries where exposure to nickel compounds
is common. The most frequent non-occupational causes of nickel derma-
titis are contact with clothing fasteners and jewelry (e.g., rivets,
snaps, earrings, costume jewelry). The actual incidence is not known,
but some sources suggest nickel is the major offender in contact sen-
sitivity to nietals.
5.1.6 Carcinogenic Dose-Response Relationships for Tvo_ Nrickel Compounds
3.1.6.1 Introduction
In this section the potential carcinogenic risk to humans due to
inhalation of either nickel carbonyl or nickel subsulfide is estimated.
Note that the carcinogenic dose-response relationships obtained here may
not be applied to pure nickel or any other nickel compounds and are
limited to inhalation exposure. Dose-response relationships were deter-
mined for these two nickel compounds because the nickel in ambient air,
in the occupational environment, and in cigarette smoke may be in the
fern of either or both of these nickel compounds.
Ideally, the carcinogenic dose-response extrapolation would be
approached from two directions:
• Given human dose-response data (generally taken from retrospec-
tive studies of past occupational exposure or of unusually high
ambient exposure levels), various extrapolation models would
be applied to obtain an approximate dose-response relationship
(a relationship giving percent excess carcinogenic response as
a function of daily dose or exposure level).
• Given dose-response data for controlled experiments on laboratory
animals, the animal doses would be converted to estimated equivalent
human doses and, again, the various extrapolation models would
be applied to obtain an approximate human dose-response relation-
sh ip.
The advantage of the first approach is that the results are of
obvious relevance to humans, since the "test" subjects are human. However,
5-23
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in retrospective studies of human exposure, the exposure levels, dura-
tion of exposure, and ever, response rates are usually only best estimates,
Unknown factors (background effects, exposure to carcinogens other than
the one in question, etc.) may seriously bias the data.
The advantage of the second approach is that the exposure, response,
and general living conditions of the laboratory animals are known since
they are design parameters or experimental variables. Also, controlled
experiments can yield a broader range of precise dose-response data
points, which allows straightforward application of the extrapolation
models, sometimes not possible based on the sparse data from human
retrospective studies. However, species differences in susceptibility,
pharmacokinetics, repair mechanisms, and the calculation of equivalent
human dose based on animal dose add considerable uncertainty to a
quantitative risk assessment.
Beyond the uncertainties associated with this type of data, there
are other important and largely unquantifiable sources of uncertainty
in this analysis.
• The main purpose of risk analysis is to extrapolate from response
rates observed at high exposure levels to response rates (risks)
at the relatively low exposure levels that might be found in
the environment. The validity of the extrapolation models,
however, cannot be tested at low exposure levels (low enough
to keep excess lifetime risk per capita around 10~5). Inade-
quate understanding of the mechanisms of carcinogenesis presents
no basis for choice among a variety of different mathematical
models. These models make similar risk predictions at high
exposure levels, but markedly different predictions at low
exposure levels. No attempt is made here to quantify the
uncertainty inherent in the choice of an extrapolation model;
rather, a variety of models are applied to establish a range
of potential risk. Also, no attempt is made to determine
statistical confidence bounds. It is felt that the quantifi-
able uncertainties inherent in this analysis would make such
a statistical exercise meaningless.
• Whether the test subjects are humans or laboratory animals, in
most cases they only very rarely have been exposed to the
carcinogen in question for an entire lifetime. To estimate
potential risk due to lifetime exposure when the exposure period
is significantly less than the lifetime of the test subjects,
a simple linear conversion is performed to determine a life-
time daily dose equivalent in mass to the actual dosage.
However, this extrapolation of intermittent or short-duration
exposure to equivalent daily lifetime exposure largely dis-
regards such factors as latency of effect, recovery by normal
repair mechanisms (i.e., existence of a true threshold level),
age-specific susceptibility (possibly due to correlated age-
5-29
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specific exposure to other toxicants), and acute toxicity at
high levels that may alter cellular defenses against a carcin-
ogenic effect. The conversion of short-term exposure to life-
time equivalent exposure may represent one of the most signifi-
cant short-comings of the risk extrapolation.
• Peculiarities, such as the lack of control groups or contra-
dictory results from equally valid studies, may make analysis
difficult. After the elimination of irrelevant or highly
questionable studies, this analysis was based on the study
whose results showed the greatest adverse effects; thus, the
analysis is conservative
In summary, the potential lifetime carcinogenic risk to humans of
a substance can be estimated by applying a variety of dose-response
extrapolation models to human dose-response data and/or to human equiv-
alent dose-response data based on laboratory animal data. Uncertainty
arises in the estimation of human exposure and response in the conver-
sion of animal exposure to human equivalent exposure, and in the appli-
cation of the dose-response extrapolation model themselves. Even
greater uncertainty arises in the conversion of short-term exposure
to equivalent lifetime exposure.
Nevertheless, in the absence of any other more acceptable method-
ologies, these procedures are currently endorsed by the EPA (U.S. EPA
I980a) . While these procedures do permit a rough quantitative approxi-
mation of risk, the predictions must be interpreted with considerable
caution.
5.1.6.2 Dose-Response Models for Estimation of Human Risk
The three dose-response models used to extrapolate human risk are
the linear "one-hit" model, the log-probit model, and the multi-state
model. The latter is actually a generalization of the one-hit model,
in which the hazard rate is taken to be a quadratic rather than linear
function of dose. All of these models are well known in the literature,
and a theoretical discussion may be found in Arthur D. Little, Inc.
(1980).
The one-hit and multi-stage models assume that the probability P(x)
of carcinogenic response to average daily lifetime dose x is described by
P(X) - 1 -e-h(x),
where h(x) is the "hazard rate" function. The log-probit model assumes
that human response varies with dose according to a log-normal distribu-
tion. Due to their differing assumptions, these models usually give
widely differing results when effects data are extrapolated from
relatively high doses to the low doses typical of environmental
exposure.
5-30
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For the linear one-hit model, the hazard rate function is h(.x)=3x -f
C, where the parameters 3 and C indicate carcinogenic response attributable
co dose x and background carcinogenic response, respectively. Solving
for 3 from the data, then the probability of carcinogenic response attribu-
table co dose x is given by
P(x) - 1 -e-Bx.
For the log-probit extrapolation, the equation
P(x) - * (A + loglo [x])
is solved for the "probic" intercept A, where * is the cumulative normal
distribution function, and ?(x) is the excess probability of response of
exposed groups over unexposed groups. This equation makes the assumption
that the log-probit dose-response curve has unit slope with respect to
the log-dose. Tables of the standard normal distribution are used to
find A, and then this value is used to determine the probability of a
response at various exposure levels.
The multi-stage model with a quadratic hazard rate function,
h(x) = ax" -i- bx ->- c,
is fit to the data, if enough are available. To estimate the parameters
a, b, and c, a maximum- likelihood method is used, aided by a computer
program which performs a heuristic search for the best fit. The para-
meter b dominates for small values of dose x, and parameter a dominates
for large values. The probability of response attributable to dose x
is then
P(x) = 1 -e
5.1.6.3 Nickel Carbonvl
For nickel carbonyl, the best carcinogenicity data (amenable to
dose-response extrapolation) currently available are from a study
on Sprague-Dawley rats administered nickel carbonyl intravenously
(Lau et al. 1972). The data selected for analysis are listed in Table
5-9. The data used are the incidences of malignant tumors at all
sites in treated and control rats.
The assumption for determining the human dose equivaJent to an
animal dose is that recommended by the EPA (U.S. EPA 1980a) , which
normalizes the dose rate according to body surface area. This approach
is relatively conservative, in that it results in a lower equivalent
human dose than would be obtained from adjusting dose on a per-kilogram
body-weight basis. Whether surface area or body weight is the more
appropriate normalization factor is open to debate.
The equivalent lifetime dose D for Che rat is simply the total dose
divided by the average lifetime of the rat (which was approximately 2
years in the study):
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TAIJLK 5-9. CARC1NOOENIC RESPONSE IN SPRAGUE-DAWLEY RATS TREATED
INTRAVENOUSLY WITH NICKEL CARBONYL
Rat Dose
20 nl/kg,
6 doses at
2-4 week
intervals
Equivalent
Human
Ingestion
Dose (mg/day)
2.5
Response
19/121
Percentage(%)
16
Percentage
Excess Over
Controls(%)
12
01
I
Oi«l/kg
0
2/47
Source: Based on data from Lau ct al. (1972)
-------
D - 20 ul/kg/dose x 6doses x 1.318
2 yr x 365 days
= 0.217 ng/kg/day
From EPA guidelines (U.S. EPA 1980a), the linear one-hit parameter B
for test animals, 3^, is given by
B - In -£ — D - 0.587 per (mg/kg/day),
Li -
where PC and P-j are the control and test group response ratios, respec-
tively. To determine the parameter 3 3 for humans, surface area adjust-
ments are made as follows:
(ng/kg/day)
- 0.05 per (ing/day) ,
where 70 kg and .3 kg are the average masses of humans and rats, respec-
tively.
In order to estimate risk due to inhalation exposure, one must
know the respiratory retention of nickel carbonyl and assume an equiva-
lence of. effect from the absorbed does by either intravenous or
inhalation routes. In the absence of the retention factor, one should
interpret the value BJJ only in terns of dose absorbed into the blood.
It cannot be assumed that ingested nickel carbonyl is equivalent to
intravenous or inhalation absorption, since the effect of gastric con-
tents on nickel carbonyl degradation is not known. In any event, in-
gestion exposure to nickel carbonyl is rare and probably does not occur
normally because of the instability of nickel carbonyl in the environ-
ment .
For the log-probit model, the human average lifetime dose DH is
derived from the animal dose D as follows:
' =0.035 mg/kg/day
= 2.5 mg/day.
Excess probability of response at dose x is,
?(x) - (19/121 - 2/47)/(l - 2/47) - 0.12
= 3 (A + logio DH)
- * (A + 0.40) ,
-1.18 = A + 0.40,
A =1.6.
Table 5-10 gives the predicted lifetime risk per capita due to absorption
of nickel carbonyl into the blood. The two models give roughly similar
5-33
-------
TABLE 5-10. PREDICTED EXCESS I.I KETIMK PER CAPITA RISK
DUE TO NICKEL CARIJONYL ABSORBED DOSE
Absorbed Dose (mg/day)
Ul
CO
Linear Model
B = 0.05 per (mg/day)
Log-Probit
Model
0.00001
5 x 10~7
off scale
0.0001
5 x 10'6
off scale
0.001
5 x 10~5
2 x 10"6
0.01
5 x 10~4
1.6 x 10~4
0.1
5 x 10~3
5 x 10~3
1
5 x l(f2
6 x 10~2
10
0.4
0.3
Source: Arthur D. Little, Inc.
-------
predictions relative to the large uncertainties in the assumptions used
in the calculations. It should be remembered that this analysis only
applies to absorbed nickel carbonyl (by inhalation or the intravenous
route) and dees net apply for any other nickel compound by any other
route.
5.1.6.4 Nickel Subsulfide
For nickel subsulfide the best carcinogenicity data (amenable to
dose-response extrapolation) currently available are from a study on
Fischer 344 rats exposed to nickel subsulfide via inhalation (Otto-
lenghi et al. 1974). The data selected for analysis are listed in
Table 5-11. The data used were the incidences of lung neoplasms in
test and control rats. The human equivalent exposure was not deter-
mined using a human-to-animal surface area ratio, such as is the normal
procedure, since inhalation minute-volume is approximately proportional
to body surface area. Thus, dose equivalence between humans and experi-
mental animals is roughly attained on the basis of body surface area when
air is breathed at the same concentration of the aerosol. This assumes
a similar disposition and retention of particulates, which is probably
not a valid assumption.
In keeping with EPA guidelines (U.S. EPA 1980a) it was assumed that
human lifetime response is related to total amount of exposure over the
rat lifetime. Assuming 104 weeks for the average rat lifetime, the
average human lifetime exposure Dr, is given by
^ / , 3s /, , -u f(6 hr/dav) x 5 dav/wk) x (78 wk) |
DH (mg/m ) - (1 ag/n^) x [(24 hr/day) x (7 day/wk) x (104 wk)J
- 0.13 rng/ra3.
From this, and the data in Table 5-11, the one-hit parameter B is
given by
1 (I - 2/215 \
" (.13 rag/n^) Vl - 29/208/
- 1.1 per rag/ra^
For the log probit model,
- $ (A -I- Iog10 [ .12
so that the probit intercept A - -0.23. The multi-stage model was not applied
because insufficient data.
Table 5-12 displays estimates of lifetime human risk based on
these values of B and A. Risk estimates are shown for exposure levels
ranging from 1 ng/n3 to 1 mg/m3. As expected, the gap between the
estimates is larger in the low-dose region; thus the model chosen
may contribute a substantial degree of uncertainty concerning the
actual carcinogenic effects of nickel subsulfide at low levels of
exposure. However, much larger contributions to uncertainty stem
from extrapolation from rat to human and estimation of the equivalent
daily exposure from a short-duration exposure.
-------
TAIJI.K 5-11. CARClNOCKNfC RKSWNSK IN FISCIIIiR 344 RATS
INHALING NLCKliL SUUSUI.l''ll)li
RaL Exposure
1 my/in ,
h hr /day,
5 day/week,
78 weeks
lujiii valent
Human .,
Kxposure (mg/m
0.13
Response
29/208
I'ercenLage (% ^
14
Excess Over
£onLj^oIs (^)
13
I
U)
0 mg/m
3
0
2/215
Source: Based on data from Ottolenghi et al. (1974)
-------
TABUS 5-12. PREDICTED EXCESS LIFETIME I'ISK-CAPITA RISK
DUE TO NICKEL SUBSULKIDE INHALATION
Air Concentration (mg/m )
Linear Model
B = .1.1 per mg/m
3
Log-Probit
Model
A = -0.23
0.000001
1 x 10
-6
off scale
0.00001
1 x 10
2 x 10
-7
0.0001
1 x 10
1.2 x 10
.... . — . . . _
0.001
1 x 10~3
6.4 x 10~4
0.01
1 x 10~2
1.3 x 10~2
O.I
1 x 10'1
1.1 x 10'1
7 x 10
-I
x 10
-\
Source: Arthur D. Little, Inc.
-------
It should be remenberad chat the results given here apply only
to nickel subsulfide by inhalation, not to pure nickel or to any
other nickel cc-pound by any ether route.
5.2 EXPOSURE
5.2.1 In t rpdu ction
Nickel is ubiquitous in the contemporary human environment such
that hunans are almost inevitably exposed to nickel in its various
chemical forms by ingestion, inhalation, and dermal contact. It has
been emphasized in the preceding sections on human health effects that
effects depend on route of exposure and species of nickel. However,
most data on human exposure do not distinguish among the various
nickel compounds. In this section, the routes of exposure are dis-
cussed separately, and, where available, speciation is indicated.
Throughout this chapter, nickel concentrations are reported in
drinking water; food; urban, industrial, and non-urban air; manmade
objects; and cigarettes.
In this section, the routes of man's exposure are identified and,
where possible, quantified. These routes are exposure through inges-
tion, exposure through inhalation, and percutaneous exposure.
5.2.2 Exposure Routes
5.2.2.1 Exposure Through Ingestion
Man may ingest nickel that is in drinking water or food, or which
is added to them either during the course of processing as a result of
contact with nickel-bearing containers, utensils, or equipment.
Nickel has been detected in groundwater and well water and in
finished drinking water supplies at low concentrations. The Community
Water Supply Study sampled and analyzed drinking water in 969 systems
serving approximately 18,200,000 persons1 (NAS 1975^ The results
of the analysis for nickel are presented in Table 5-13; the average
nickel concentration found in these water supplies was 4.8 mg/1.
Other studies of tap water and well water in the United States
found average concentrations of nickel in the range of 2.3 ug/1 to
13.0 i.g/1, as shown in Table 5-14. All means reported here were below
the established water quality criterion of 13.4 yg/1. For coinparsion,
the mean nickel concentration in drinking water in the heavily industrial
city of Sudbury, Ontario is 200 yg/1, however, this is not to be con-
sidered at all typical of concentrations in water supplies in the
United States.
'"This study took place in 1963 at which time there were 19,236 public
water supply systems serving approximately 150 million persons in
the United States.
5-38
-------
TABLE 5-13. NICKEL IN DRINKING WATER SUPPLY SYSTEMS
IN THE UNITED STATES
Nickel Content (••§/!) Sauiules
<0.9
1 -
6 -
11 -
16 -
2i _
26 -
31 -
36 -
41 -
46 -
51 -
75
5
10
15
20
25
30
35
40
45
50
55
543
1082
640
167
46
14
4
9
1
1
1
1
1
Frecuency of Detection (%)
21.69
43.22
25.57
6.68
1.84
0.56
0.16
0.08
0.04
0.04
0.04
0.04
0.04
Total 2503 100.00
Average concentration 4.8 ug/liter
Note: Covers all 969 water supplies in eight metropolitan areas
and one state.
Source: NAS (1975)
5-39
-------
TABLE 5-14. NICKEL LEVELS IN DRINKING WATER
Survev
Tao Water
Mean Maximum Number of
(ug/1) (-j g/1) Systems Samples Reference
8 Metropolitan Areas 4.8
(1969-1970)
10 Largest U.S. Cities 2.3-13.0'
(1972)
Hartford, CT
Sudbury, Ontario
75
1.1
200
1.5
264
969
NAS (1975)
Dufor and Becker
(1964)
McNeely et al. (1972)
McNeelv et al. (1972)
Well Water, typical
Well Water, maximum
in Ohio River Basin
1978 and 1979
10 50
31,700b
U.S. EPA 1980b
U.S. SPA 1980b
aew York City; Philadelphia; Chicago; Los Angeles; Detroit; Houston;
Baltimore; Dallas; San Diego; and San Antonio.
This value was reported in only one sample and is not considered represen-
tative of the maximum nickel concentrations in U.S. drinking waters.
5-40
-------
Typical naxirnutn concentrations reported in the literature (MAS
1975) and in the STORET !;atar Quality System (U.S. EPA 19SOb) were in
the range of 1.5 ug/1 to 75 -g/1. Exceptionally high concentrations
were reported in certain, well ss.ir.nles in the Ohio River Basin on isolated
occasions in 1978 and 1979; these were 31,200 ug/1 and 31,700 ug/1
(U.S. EPA 1980). There is no information available on the number of
persons served.
It has been estimated that man drinks an average of 2 liters of
wacer per day. The daily intake contributed by drinking water Co ingested
nickel would be an average of 4.6 yg to 26 ug per day, with a typical
maximum contribution in the United States of less than 150 ug/day.
Xickel is found in food as a result of its occurrence in the environ-
mental media through man's activities and natural phenomena. Nickel
occurs naturally in soil and is deposited through atmospheric fallout
and waste disposal to land; nickel occurs in water due Co erosion of
rocks and soils and also from atmospheric fallouc. The nickel in soil
and water is taken up by most organisms and is passed from zooplankton,
p'nytoplankton, and plants to higher forms of life.
The nickel levels found in harvested crops are dependent primarily
on the crop and less on the concentration of nickel in soil and
soil characteristics. Leafy vegetables, such as lettuce and grass-like
plants, usually contain the highest nickel levels of crops. There does
not appear to be any particular affinity of nickel for fruits, seeds,
or other high lipid plant constituents.
In most crops grown in sludge-amended soils, nickel concentrations
do not usually exceed 4 ug/g. Lettuce and wheat tend to have higher
levels, on the order of 10-200 yg/g (see Table 4-14 in Chapter 4.0).
Unusually high concentrations were measured under laboratory conditions.
Under low pH conditions, which could easily develop in unmanaged sludge-
treated sites, concentrations increase dramatically to levels as high
as 1150 ug/g in lettuce and 4000 ug/g in allysum (a forage crop). No
field study of a sludge-amended plot found comparable levels. Until
such time as these results are verified in the field, these concentrations
cannot be considered representative of foods grown in sludge-amended
soils. However it is likely that the concentration of nickel will be
higher in sludge-treated soils than in non-treated soils. The behavior
of nickel in plants and organisms is more fully discussed in Section
4.4 - Biological Fate.
Xickel occurs as a trace element in many foods that man consumes.
The nickel concentration is reportedly high in green leafy vegetables,
grains, tea, herring, and oysters and, as noted above, is likely to be
higher in crops treated with sewage sludge (Schroeder et al. 1961,
Underwood 1971). A sample of foods containing nickel and associated
concentrations is presented in Table 5-15. A nore detailed analysis
of nickel in foods is found in Table 4-14.
5-41
-------
TABLE 5-15. NICKEL CONCENTRATION IN VARIOUS FOODS
FOOD GROUP
Dairy
Heat, Fish, Poultry
Grains
Potatoes
Leafy Vegetables
Legume Vegtables
Garden Fruits
Root Vegetables
Fruits
Oils and Fats
Sugars
Beverages
AVERAGE CONCENTRATION
NICKEL (ug/8)
0.00-0.03
0.00-4.50
0.00-6.45
0.56
0.14-1.14
0.17-2.55
0.03-0.33
0.37-1.94
0.00-0.34
0.00-1.14
0.03
0.00-7.60
SOURCE: Schroeder et al. (1961)
5-42
-------
Nickel in food due to leaching from processing equipment: is another
sourca of ingesced nickel. Depending on che pH of Che food, there is
a potential for corrosion of nickel-alloy vessels during use. Many
stainless steels (most containing nickel) have been shown to lack cor-
rosion resistance (MAS 1975). Equipment used in milling flour and
wheats is likely to add nickel to end-products such as breads.
There is little infomation available on the chemistry of nickel
in foods. It is therefore impossible to realistically determine the
bioavailability and biotoxicity of nickel in foods. However, the
nickel contribution in foods eaten by man has been calculated.
Oral intakes of nickel as a result of food consumption has been
determined by several studies and is summarized in Table 5-16. The
average amount of nickel consumed in the daily diet ranged from 165
•_g to 900 ug. There is apparent variation between the diet of males
and females, the latter being higher in nickel, as indicated by Tipton
and coworkers (Tipton _e_t al. 1966) . While the Tipton study was an
isolated study of only one male and one female, it provided thorough
documentation and was included as a basis for comparison.
5.2.2.2 Exposure Through Inhalation
Man nay be exposed by inhalation to nickel in ambient air and in
cigarette smoke. Nickel occurs in the atmosphere as a result of
industrial activity, combustion of fossil fuels, or other human
activities in the urban environment. In the rural environment, nickel
occurs in the air largely as a result of wind erosion of nickel-bearing
soils. The species of nickel in ambient air have not been identified.
Nickel in cigarette sraoke, on the other hand, is believed to be mostly
nickel carbonyl. Because of this distinction, the two inhalation
exposure routes are discussed separately.
Nickel is commonly detected in the atmosphere surrounding urban
areas. Sources of nickel include combustion of petroleum fuels, which
contain up to 50 aig/1 nickel (Acurex 1980) ; combustion of coal, the
ash of which contains 3 to 10,000 mg/kg nickel (Schroeder et. al. 1970);
and particulates from the exhausts of non-diesel vehicles, which contain
500 to 10,000 mg/kg nickel (Schroeder et al. 1970). The concentration
that this corresponds to in air has not been determined.
There are several studies which present concentrations of nickel
in urban air and these are summarized in Table 5-17. In a study of 58
cities by Schroeder e_t_ al. (1961), the range of nickel concentrations in
urban air was 1 to 118 ng/rr.3, with two-thirds of the locations sampled
being less than 20 ng/mj.
A seasonal variation in nickel concentration in the urban environ-
ment has been determined in one study reported by the National Academy
of Science (1975). The results are shown in Table 5-18. Nickel was
5-43
-------
TABLE 5-16. NICKEL IN THE HLTLAN DIET
COMPARATIVE DIET
2300-Calorie Diet
Institutional Diet
in United States
Institutional Diet
in United States
Institutional Diet
Children 9-12 years
old
Dietary Analysis of
Husband and Wife:
Male
Feaale
American Adults
AVERAGE NICKEL IN TEE DIET
(ug/Jay)
700-900
472
165
451
170
330
500
REFERENCE
Schroeder et al. (1961)
Schroeder et al.
Myron et al. (1961)
Murthy e_L al. (1973)
Tipton _et_ al. (1966)
Tipton Bt_ al_. (1966)
Louria et al. (1972)
5-44
-------
TABLE 5-17. NICKEL IN URBAN AIR
Description
Ten Cities Studied
Year-Round
Colder Months
Wanner Months
Range
(ng/m.3)
30-120
Mean When
Available
(ng/m3)
44
26
Reference
Schroeder et al. (1970)
Schroeder et_ al. (1970)
Schroeder et al. (1970)
Urban Air
56 Cities Detected
of 58 samoled
1-118
Schroeder ec al. (1970)
Urban Air
Boston Air
East Chicago Air
Philadelohia Air
up to 690
32
112
132
78
Sullivan (1969)
NAS (1975)
MAS (1975)
NAS (1965)
Cities include New York City; Rochester, NY; Bayonne, NJ; Portland,
OR; Somerville, MA; New Haven, Hartford,and Bridgeport, CT; Bakersfield,
Burbank, and San Bernadino, CA; Baltimore, MD.
5-45
-------
TABLE 5-18. SEASONAL VARIATION OF NICKEL DI AMBIENT AIR
Urban Air Non-Urban Air
All Year 21 6
Fall and Winter 25 6
Spring and Summer 17 6
Source: NAS (1975)
5-46
-------
detected at concentrations alaosc 50% higher in the fall and winter
months than in the spring and summer months. Nickel in the rural
environment did not appear to vary between seasons.
Nickel is contributed to the general urban environment as a result
or coal and petroleum combustion for power generation and utilization of
petroleum for space heating. The population in the vicinity of these
point sources is exposed to greater concentrations of atmospheric
nickel. Samples of stacks from coal-fired Dower plants indicate that
nickel concentrations range from 13-65 ug/nH (Lisk 1972). The same
study sampled petroleum-burning plant emissions and determined nearby
atmospheric concentrations of 63 to 447 ug/m^.
The associated atmospheric nickel concentrations to which the
nearby populations are exposed would clearly be significantly lower
as the particles disperse through the air, the heavier ones falling
out on the land. Sampling data were not available to identify the
species of nickel resulting from these emissions or to identify the
associated concentrations.
Non-urban atmospheric concentrations of nickel are clearly lower
than in the urban and industrial environments. The mean concentration
of nickel reported in a study of 47 non-urban areas by the National
Air Surveillance Networks (MASK) was 6 ng/n3 (MAS 1975). Other
studies reported (MAS 1975) concur with the NASN results that the ratio
of nickel in urban air to that in non-urban air is typically 2:1.
To summarize inhalation exposure through ambient air, nickel
concentrations range from 0.6 ng/ra^ to 690 ng/tu^ in most environ-
ments and are possibly higher near industrial emitters of nickel;
these levels are shown in Table 5-19. Although average inhalation rates
have been determined (1.8 ra-V'nr) , without identifying the species of
nickel inhaled, its absorption rate and location cannot be determined.
It is difficult to estimate the actual amounts of nickel absorbed via
inhalation without data on speciation, particle size, and actual deter-
mination of respiration retention for each species.
Nickel is found in the leaves of tobacco products used for cigarettes,
Stahly (1973) reported that nickel carbonyl occurs in cigarette smoke
at concentrations of 0.35-1.8 ug Ni per liter of smoke, which is
approximately 1.5 yg nickel carbonyl per cigarette (assuming 14 puffs
of 36 milliliters each). Most of the nickel contained in an average
cigarette remains in the ashes, butt, and filter. These measurements
are consistent with the hypothesis that the nickel carbonyl is formed
in the cooler zones of the cigarette behind the combustion zone by
combining the nickel in the tobacco, the paper, and the CO produced
from the burning tobacco. Nickel was removed from tobacco by passing
CO through it at temperatures between 20 and 100°C. The inhalation
retention for nickel carbonyl is uncertain, but, assuming a retention
of 50^, a one-pack-a-day sr.oker nay absorb 15 pg/day or about 5 mg/yr
5-47
-------
TAIJLI-: 5-19. NfCKIil. CONCKNTRATIONS IN AMIMKNT AIR
Ul
I
do
Non-Urban Air
Non-Urban Air
Urban Air
At the Point of
(•'.mission of Com-
bustion Plants
Coal Combustion
Petroleum Combustion
Mini mum
(ng/m3)
0.6
1.0
12,900C
63,000C
Max imum
(ng/m3)
12.0
690.0
65,000°
447,000a
Mean
(ne/in3)
6.0
Reference
See Sect ion 4.5.5.')
NAS (1975)
See Table 5-17
l.iak (1972)
l.isk (1972)
3Note: Assoeiatetl atmospberic levels beyond tbe stacks will be significantly lower.
-------
of nickel carbonyl. The actual amount of nickel carbonyl absorbed when
smoking would also depend on puffing rates and brand of tobacco. Stahly
(1973) suggests there nay be practical ways to remove nickel from tobacco
j^
aroducts.
5.2.2.3 Cu t an e o us Exposure
The use of nickel-containing commodities which permit cutaneous
exposure to nickel is legion and was estimated to be increasing by
about 10% per year (NAS 1975). The major sources of environmental
cutaneous exposure to nickel are jewelry, coinage, clothing fasteners,
tools, cooking utensils, stainless steel kitchens, and detergents. At
issue is which sources are most likely to be involved in the sensitiza-
tion of people to nickel and which sources may only be involved in con-
tinued sensitivity reactions.
There seems little doubt that sensitization arises in susceptible
individuals due to exposure to coinage (especially cashiers), jewelry,
and nickel-plated garment fasteners. More controversial is the role
of nickel in detergents in causing or even eliciting a response in
sensitive individuals. Studies cited by NAS (1975) reported nickel
content of detergents of less than 10 mg/kg, which levels were thought
not adequate to produce sensitization. Exposure to nickel from stain-
less steel kitchens has not been investigated carefully for its potential
to produce sensitization.
Fischer (1967) has stated that sweating has a profound affect on
the degree of dermatitis and is required for sensitization to nickel.
It is hypothesized that nickel combines or is solubilized by sweat,
diffuses into sweat ducts and hair ostia, and subsequently into dermis,
where it combines with components of the skin and soluble proteins.
The resultant nickel "complex" is an antigen which stimulates an
immunological response (NAS 1975). Further research is necessary to
clarify details of this hypothesized scenario.
An association between nickel in ambient air or nickel ingestion
and contact sensitivity has not been suggested. Two cases of Loftier's
syndrome (pulmonary eosinophilic) have been reported (Sunderman and
Sunderman 1961) which were each associated with exposure to nickel
carbonyl. One of the individuals was subjected to a nickel patch-
test and found to be very sensitive.
5.2.3 Suninary
Nickel exposure through ingestion of drinking water does not
appear to be a significant route due to the generally low concentrations
of the metal found in well waters and treated drinking water systems.
Except in rare instances, drinking water concentrations were below the
established Water Quality Criterion of 13.4 ng/l. Nickel exposure
5--9
-------
through oral intake of food typically contributes 100 ug to 990 ug to the
daily diet, however, nothing is known about its chemical form. Nickel
in ambient air occurs in fairly low concentrations ranging from 0.6
ng/ir. to 690 ng/nH and most frequently between 100 ng/m-' to 200 ng/raX
In areas near intense industrial activity with associated high nickel
emissions, the nickel concentrations are higher but speciation is unknown.
Cigarette smoking may contribute 15 ug/day of nickel carbonyl to the
average one-pack-a-day smoker. Finally, percutaneous exposure occurs
as a result of contact with nickel-bearing objects (e.g., stainless
steel kitchenware, jewelry). Upon repeated contact with such objects,
the skin of some individuals may become sensitized, however more study
is needed on the grade of alloy from which these objects are made and
the associated releases of nickel.
=>~50
-------
REFERENCES
Acurex Corporation. Materials Balance for Nickel. Rosslyn, VA: Acurex
Cor?; 1930.
Adalis, D. ; Gardner, D.E.; Miller, F.J. Cytotoxic effects of nickel on
ciliated epithelium. Amer. Rev. Resp. Dis. 118:347-354; 1978.
Adkias, 3., Jr.; Richards, J.H. ; Gardner, D.E. Enhancement of experi-
mental respiratory infection following nickel inhalation. Environ.
Res. 20:33-42; 1979.
Ambrose, A.M.; Larson, ?.S.; Borzelleca, J.R.; Kennigar, G.R. Long ^
tern toxicologic assessment of nickel in rats and dogs. J. Food Sci.
and lechnol. 13:181-187; 1976. (As cited in U.S. EPA 1979)
Aranil, D. ; Miller, F.J.; Andres, S.; Ehrlich, R.; Fenters, J.; Gardner,
D.E.; Waters, M.D. Cytoxicity to alveolar marcrophages of trace metals
adsorbed en fly ash. Environ. Res. 20:14-23; 1979.
Arthur D. Little, Inc. Integrated exposure risk assessment methodology.
Draft. Contract 68-01-3857. Washington, DC: Monitoring and Data Support
Division, U.S. Environmental Protection Agency; 1980.
Beach, D.J.; Sunderman, F.W. Nickel carbonyl inhibition of RNA synthesis
bv a chromatin-RNA polymerase complex from hepatic nuclei. Cancer Res.
30:48-50: 1970.
3ernacki, E.J.; Parsons, G.E.; Roy, B.R.; Mika-Devic, M.; Kennedy, D.C.;
Sunderman, F.W., Jr. Urine nickel concentrations in nickel-exposed
workers. Ann. Clin. and Lab. Sci. 8:184-189; 1978.
Camner, P.; Johansson, A.; Lundborg, M. Alveolar macrophages in rabbits
exposed to nickel dust. Environ. Res. 16:226-235; 1978.
Costa, M.; Mollenhauer, H.H. Carcinogenic activity of particulate nickel
compounds is proportional to their cellular uptake. Science 209:515-
517; 1980,
Costa, M.; Nye, J.S. Sunderman, F.W.; Allpass, P.R.; Gondos, B.
Induction of sarcomas in nude mice by implantation ot Syrian hamster
fetal cells exposed in vitro to nickel subsulfide. Cancer Res. 39:
3591-3597; 1979.
DiPaolo, J.A.; Caste, B.C. Quantitative studies of in vitro morphological
transfor-ation of Syrian hamster cells by inorganic netal salts. Cancer
Res. 39:1008-1013; 1979.
Doll, R.; Morgan, L.G.; Speizer, F.E. Cancers of the lung and nasal
sinuses in nickel workers. Brit. J. Cancer 24:623-632; 1970.
Dufor, C.N.; Becker, E. Public water supplies of the 100 largest cities
in the United States, 1962. U.S. Geological Survey Water Supply Paper
No. 1812, Washington, DC: U.S. Government Printing Office; 1964.
Farrell, R.L.; Davis, G.W. The effects of particulates on respiratory
carcinogenesis by diethyl nitrosamine. Karbe, !.; Park, J.F. eds.
Experimental Lung Cancer: Carcinogenesis and bioassays, New York, NY:
Springer-Verlag; 1974, pp. 219-233. (As cited in IARC Vol . 11, 1976)
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-------
Fisher, A.A.; Contact Derraaticis; Philadelphia: Lau and Fefaiger, pp.
324; 1967. (AS citsd in U.S. EPA 1979, NAS 1975)
Grahs.ni, J.A., Gardner, D.E.; Waters, M.D.; Coffin, D.L. Effect of
trace metals on phagocytosis by alveolar macrophages. Infection and
Immunity 11:1278-1233;'1975.
Greenblatt, D.J.; Kock-Weser, J. Clinical Pharraacokinetics, Part I.
NEJM 293:702-705; 1975.
Heath, J.C.; Webb, M.; Caffrey, M. Interaction of carcinogenic metals
with tissue and body fluids, cobalt and horse serum. 3r. J. Cancer
23:153; 1969. (As cited in Webb and Weinzieri 1972)
Horak, E. ; Sunderman, F.W. Fecal nickel excretion by healthy adults.
Clin. Chem. 19:429-430; 1973. (As cited in NAS 1975).
Ho, ".; Furst, A. Nickel excretion by rats following a single treatment.
Proc. West. Pharmacol. Soc. 16:245-248; 1973. (As cited in U.S. EPA
1979)
Hoey, M.J. The effects of metallic salts on the histology and functioning
of the rat testes. J. Reprod. Fertil. 12:461-471; 1966. (As cited in
U.S. EPA 1979)
Hueper, W.C. Experimental studies in metal carcinogenesis. Arch. Pathol.
65:600-607; 1958*.
Hueper, W.C.; Payne, W.W. Experimental studies in metal carcinogenesis;
chromium, nickel, iron, and arsenic. Arch. Environ. Health 5:445-462;
1962. (As cited in IARC 1976)
International Agency for Research on Cancer (IARC). Nickel and nickel
compounds. In: Evaluation of Carcinogenic Risk of Chemicals to Man
(International Agencv for Research on Cancer Monographs) Lyon,
pp. 111. 23, 75-112; 1976.
International Radiological Protection Commission (IRPC). Task group on
lung dynamics for Committee II. Deposition and retention models for
internal dosimetry of the human respiratory tract. Health Physics
12:173-207; 1966.
Johansson, A.; Camner, P. Are alveolar macrophages translocated to the
lymph nodes? Toxicology 15:157-162; 1980.
Kasprzak, K.S.; Sunderman, F.W. The metabolism of nickel carbonvl C.
Toxicol. Appl. Pharmacol. 15:295-303; 1969.
Kasprzak, K.S.; Marchow, L. ; Breborowics, J. Pathological reactions
in rat lungs following intratracheal injection of nickel subsulfide
and 3,4-benzpyrene. Res. Comm. Chem. Pathol. Pharmacol. 6:237-245; 1973.
5-52
-------
Kincaid, J.F.; Strong, J.S.; Sunderman, F.W. Nickel poisoning. I.
Experimental study of the effects of acute and subacute exposure to
nickel carbonyl. Arch. Ind. Hyg. Occup. Med. 8:43-60; 1953.
Kreyberg, L. Lung cancer In vorkers in a nickel refinery. Brit. J.
Ind. Med. 35:109-116; 1978.
Langer, A.M.; Rohd, A.N.; Selikoff, I.J. Asbestos as a cofactor in
carcinogenesis among nickel-processing workers. Science 209:420-422;
1980.
Lau, T.J.; Hackett, R.L.; Sunderman, F.W. The carcinogenicity of
intravenous nickel carbonyl in rats. Cancer Res. 32:2253-2258; 1972.
Lisk, D.J. Trace metals in soils, plants, and animals. Advances
Agron. 24:267-365; 1972.
Louria, D.B.; Joselow, M.M.; Browder, A.A. The human toxicity of
certain trace elements. Ann. Int. Med. 76:3-7-319; 1972.
McNeely, M.C.; Nechay, M.W.; Sunderman, F.W. Measurements of nickel
in serum and urine as indices of environmental exposure to nickel.
Clin. Chem. 18:992-995; 1972.
Murthy, G.D.; Rhea, U.S.; Peeler, J.T. Levels of copper, nickel,
rubidium, and strontium in institutional total diets. Environ. Sci.
Technol. 7:1042-1045; 1973.
Myron, D.R.; Zimmerman, T.J. ; Shuler, T.R.; Klevay, L.M.; Lee, D.E.;
Nielsen, F.H. Intake of nickel and vanadium by humans. A survey of
selected diets. Am. J. Clin. Nutr. 31:527-53l"; 1978.
National Academy of Sciences (NAS). Nickel. Washington, DC: National
Academy of Sciences; 1975.
Nishimura, M. ; Uraeda, M. Induction of chromosome aberrations in cultured
naranialian cells by nickel compounds. Mut. Res. 63:337-349; 1979.
Onkelinx, C.J.; Becker, J.; Sunderman, F.W. Compartmental analysis of
the metabolism of °^Ni(II) in rats and rabbits. Res. Comm. Chem. Pathol.
Pharaacol. 6:663-676; 1973.
Oskarson, A.; Tjalve, H. An autoradiographic study on the distribution
of 63NiCl2 in mice. Ann. Clin. Lab. Sci. 9(l):47-59; 1979a.
Oskarson, A.; Tjalve, H. The distribution and metabolism of nickel
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5-53
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5-54
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5-55
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5-56
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6.0 EFFECTS AND EXPOSURE — AQUATIC ORGANISMS
In this chapter, the effects of nickel on aquatic organisms are
considered within the context of the available exposure data.
6.1 EFFECTS
6.1.1 Introduction
This section provides information about the levels of nickel at
which the physiologic processes and normal behavior of aquatic organisms
are disrupted.
Nickel is a common component of natural waters and may be found in
"unpolluted" waters at levels less than 1 ug/1 (U.S. EPA 1980b). It
is possible that nickel is an essential element to biota in trace amounts
(probably low ug/1 range or lower), but the threshold of toxic effects
to freshwater organisms is in the range of 1 ug/1 to 10 ug/1. In
an aqueous environment, nickel may exist, albeit infrequently, in the
very insoluble elemental form. The more common form in waters is the
free divalent nickel ion (Ni++) , resulting from one of the nickel salts
(e.g., nickel chloride, nickel sulfate, nickel ammonium sulfate) or
one of many other nickel compounds or complexes. In toxicity test
systems, with low concentrations of suspended solids and dissolved
organic matter, the most prevalent form of nickel is the Ni++ free form.
Nickel salts are very soluble in distilled water; however, in natural
waters their solubility varies with such water quality parameters as pH,
hardness, and alkalinity. The solubility of nickel salts in general
decreases with increasing water hardness, a factor which greatly affects
the toxicity of nickel to aquatic organisms under both natural and
experimental conditions. Toxicity tests have shown that as water
hardness increases, toxicity of nickel to aquatic organisms decreased
(U.S. EPA 1980a).
Although more than 180 organonickel compounds and nickel complexes
are commercially available in the United States, studies to determine the
mechanisms of toxicity have been conducted on only a few of them, and
most of these studies have been performed on laboratory mammals. Nickel
in the elemental form is considered not to be very toxic, and is generally
passed through systems, such as sewage treatment plants and individual
organisms, essentially unchanged. Nickel salts have been observed to
be highly toxic to laboratory mammals when injected, but when orally
ingested more than 90% of the nickel was excreted (NAS 1975). From
studies conducted by Schweiger (1957) of the acute effects of nickel
(Ni++) on several riverine fish species, it was observed that mortality
was caused by suffocation, with paralysis preceding death. Histological
examination showed respiratory gill obstruction by mucous matter expelled
from the cells.
6-1
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6.1.2 Freshwater Organising
6.1.2.1 Acute Effects
The acute effects of nickel have been tested in numerous freshwater
organisms. Many of the organisms were studied under varying conditions
of water hardness (mg/1 as CaC03>. Water hardness greatly affects the
toxicity of nickel to biota and, in general, as hardness increases, an
organism's resistance to toxicity increases. This toxicity difference
between hard and soft water is due to the fact that absorption of
trace metals from the environment by biota is inversely related to the
concentration of calcium (Hutchinson and Collins 1978). Natural levels of
nickel in freshwater have been found to range from 0.003 mg/1 to 0.086 mg/1
(U.S. EPA 1980b). Of the freshwater fish tested, the most sensitive species
is the fathead minnow (Fimphales promelas) ; ^£50^ values in soft water
were 3-5.1 mg/1. Hard water toxicity values were much higher, in the
25-45 mg/1 range. The goldfish (Carossius auratus) and guppy (Lebistes
reticulatus) were also sensitive to nickel in the range of 4-10 mg/1
in soft water. Toxicity data for several freshwater fish are summarized
in Table 6-1.
Of the freshwater invertebrates studied, the zooplankton (cladocera,
copepod, and rotifers) and two aquatic insects were killed by nickel at
somewhat lower concentrations than were the most sensitive fish species
(LC5Q range of 1-4 mg/1). The snail Amnicola spp., the bristleworm, and
several other aquatic insects had LC$Q values of 14.3, 14.1, and 28-33
mg/1, respectively. The available data for acute toxicity to freshwater
invertebrates are summarized in Table 6-2.
Several freshwater algae species have been studied for nickel
toxicity. Reduced growth occurred in four species tested at concen-
trations in the range of 0.100-0.700 mp/1 (see Table 6-3). In mixed algae
populations, a decrease in diatom diversity and a population shift to
blue-green algae was observed in 0.002-0.0086 mg/1 of nickel (U.S. EPA 1980a)
Freshwater toxicity data for several other nickel compounds are
summarized in Table 6-4.
6.1.2.2 Chronic Effects
Chronic or sublethal effects of a toxic substance in aquatic organ-
isms are generally determined by observing effects such as loss of
equilibrium, melanization, narcosis, swollen hemorrhaging gills, and
changes in reproductive or feeding habits or capabilities.
Fathead minnows exposed continuously from age 6 weeks until they
spawned to a concentration of 0.73 mg/1 NiCl2 showed no effect on growth
LC5Q is the concentration that is lethal to 50% of the test organisms.
6-2
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TABLE 6-1. ACUTE TOXIClTY OF NICKEL - FRESHWATER FISH
Bioassay*
Organism Method
American eel S
Anguilla rostrata
Brook Trout S
Salvelinus tontinalis
Rainbow Trout S
3aLno gatrdneri
Rainbow Trouc S
Salao gairdneri
Lake Trout S
Saivelinus naraavcush
Goldfish S
Carassius auratus
Fatheadmitvnow S
Pimeoha es promelas
Fathead minnow S
Plaepha les protn_elas
Fatheadminnow S
Pimeohales pronelas
Fathead minnow FT
Pinephales promelas
Carp S
Cvprinus carpio
Channel catfish S
Ictaluois punctatas
Hardness
(ag/1 as CaC031
55
42
240
42
42
20
210
20
360
29
55
42
Tiae 1C 50
i (hrs) (pg/1)
96 13.0
48 53.9
43 32.0
48 35.7
48 16.7
96 9,8
96 27.0
96 5.2
96 44.5
96 2.9
96 10.4
43 36.8
Reference
Rehwoldt et al. (1972)
Millford (1966)
Brown and Dalton (1970)
Wlllford (1966)
Willford (1966)
Pickering and Henderson
(1966)
Pickering (1974)
Pickering and Henderson
(1966)
Pickering and Henderson
(1966)
Lind et, al., (no date)
Rehwoldt et al. (1972)
Willford (1966)
Banded kill!fish S
Fundulus diaphanus
55
96
46.1
Rehvoldt e£ al^ (1972)
6-3
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TABLE 6-1. ACUTE TOXICITY OF NICKEL - FRESHWATER FISH (CONTINUED)
Bioassay
Organism Method
Guppy S
Lebistes reticulatus
Rock bass FT
Ambloolites rucestris
Striped bass S
Hardness
(rag/1 as CaC03
20
26
53
Time
(hrs)
96
96
96
LC50
(mg/1)
4.4
2.5
6.2
Reference
Pickering and
Henderson (1966)
Lind et al. (no dace)
Rehwoldt _e_t al. (1971
Roccus saxatilius
Pumpkinseed S
Lepomis gibbosus
Bluegill S
Lepomis macrochirus
Bluegill S
Lepomis macrochirus
Bluegill S
Lepomis macrochirus
White perch S
Roccus Americanus
20
360
42
53
96
96
96
48
96
8.0 Rehwoldt et al. (1972)
5-2 Pickering and
Henderson (1966)
39.6 Pickering and
Henderson (1966)
110.4 Willford (1966)
13.6 Rehwoldt et al. (1971)
oioassay Method:
S - Static; test organisms are exposed to a single concentration of the pollutant
in a fixed volume of water in order to simulate an accidental exposure.
FT » Flow through; fixed concentration in continually flowing water to simulate a
constant source of pollutant (e.g. a discharge).
6-4
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TABLE 6-2. ACUTE TOXICITY 0? NICKEL - FRESHWATER INVERTEBRATES
Sioassay3
Organisn Method
Rotifer
Philodina acucicornus
Bristle worm
Mais sp
Snail (egg)
Ann i co la sp.
Snail (adult)
Amnicola sp.
Cladoceran
Daphnia hyalina
Cladoceran
Daphnia magna
Cladoceran
Daphnia pulicaria
Cladoceran
Daphnia pulicaria
Copepod
Cy c lops abyssorum
Copepod
Eudiapcomus padanus
Scud
Gamnarus sp.
Mayfly
Ephemerella subvaria
Stonefly
Acroneuria lycorias
Damself ly
(unidentified)
Midge
Chironomus sp.
Caddisfiv
(unidentified)
R
S
S
S
S
S
R
R
S
S
S
S
S
S
S
S
Hardness
(aig/1 CaC03)
25
50
50
50
45
29
244
50
42
50
50
50
50
Time
(hrs)
96
96
96
96
48
48
48
48
48
48
96
96
96
96
96
96
LC50
(jig/1) Reference
2.9 Buikeraa ec al. (1974)
14.1 Rehwoldt et al.(1973)
11.4 Rehwoldt et al. (1973)
14.3 Rehwoldt et al . (1973)
1.1 Baudoin and Scoppa (1974)
0.5 Biesinger and Christensen
(1972)
O-7 Lind et_al_._(no date)
3.8 Lind et al. (no date)
15 Baudoin and Scoppa (1976)
3.6 Baudoin and Scoppa (1976)
13 Rehwoldt et al. (1973)
4.0 tfaimick and Bell (1969)
33.5 Mamlck and Bell (1969)
21.2 Rehwoldt et_ aT._ (1973)
8.6 Rehwoldt et al. (1973)
30.2 Rehwoldt et al. (1973)
Bioassay Method:
5. » Renewal; variation of a staci:
S - Static
cesc with repeated exposure.
6-5
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TABLE 6-3. EFFECTS OF NICKEL ON FRESHWATER PLANTS
Organism
Alga
Ch1amyd omona s
euganetos
Alga
Chjorella vulgaris
Alga
Haamatococcus
caaensis
Alga
g_cenedesmu3
acuminata
Alga
Scenedes-ius
acuminata
Effect
Reduced growth
Reduced growth
Reduced growth
Reduced growth
Reduced growth
Concentration
(mg/1)
0.7
0.5
0.3
0.5
0.1
Reference
Hutchinson (1973)
Hutchinson (1973)
Hutchinson (1973)
Hutchinson and Stokes
(1975)
Hutchinson (1973)
6-6
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TABLE 6-4. FRESHWATER TOXIC1TY - OTHER NICKEL COMPOUNDS
Nickel chloride
Organism
Gold fish
Carassius a,uratus
Guppy
Lebistes reticulatus
Fathead minnow
Dimephales promelas
Fathead minnow
Pirnephales oromalas
Daphnia magna
Bluegill
LepOTnis raacroc'nirus
Bluegill
Lep_omis macrochirus
E. coli
Water
Condition
Time Concentration
Ors) (mg/1) Effect
Stickalback
Rainbow Trout
Salmo gairdneri
Brown Trout
S a lino trutta
Brook Trout
Salvelinus^ fontinalis
Lake Trout
Salvelinus mamycush
Chanel Catifish
Ictalurus punctatus
Mayfly
Ephemerella s?.
Stonefly
Acroneuria Ivcorias
soft
soft
hard
soft
hard
200
96
96
96
96
96
4.5
4.45
4.0
24
6.0
(As N:)
5.18
39.6
0-1
Nickel Sulfate
49
48
48
48
48
48
50
160
270
242
75
165
Lethal
thresnold
threshold
concentration
Lethal
96
33.5
6-7
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TABLE 6-4. FRESHWATER TOXICITY - OTHER N'ICKEL COMPOUNDS (CONTINUED)
Nickel Ammonium Sulfate
Organism
Daphnia magna
E. Coli
Scenedesmus
Concentration
(mg/1)
6(Ni)
0.1
0.09
Effect
Deleterious Effect
Toxic Threshold
Toxic Threshold
Nickel Nitrate
Organism
Stickleback
Stickleback
Stickleback
Concentration
(mg/1)
2.44
1.5
0.8
Effect
Threshold Concentration
Lethal Concentration (96hr)
Lethal Concentration(24hg)
iLrn * median tolerance limits.
Source: U.S. EPA (no date)
6-3
-------
and survival, but a significant reduction in the number of eggs per
spawning incidence and on che hatchabiiity of the eggs was observed
(Blayiock and Frank 1979).
In experiments with carp (Cyprinus carpio) eggs and larvae, there
was no effect on hatchabiiity of the eggs in concentrations of nickel
up to 4 mg/1. At 6 mg/1, only 50% of the eggs hatched, with no further
decrease in percentage hatched through 7 mg/1 nickel. At concentrations
greater than 7 mg/1, embryonic development continued through the eyed-
embryo stage, but the number of eggs hatched decreased until at 10 mg/1
only 3 larvae, which were abnormal, hatched from 414 eggs. At concen-
trations greater than 30 aig/1, no embryonic development was observed
(Blaylock and Frank 1979).
6.1.3 Mar ine Or g an i sms
Toxicity data for marine biota are not extensive, and there is even
less data for fish than for invertebrates. Background concentrations
of nickel in sea water were found to be approximately 0.0054 mg/1 (U.S.
EPA1980b).( The most sensitive fish species tested was the Atlantic
Silverside, LCrQ of 14.6 mg/1. Other values are 33 tng/1 for the winter
flounder, and 350 mg/1 (96 hr) for the Munnnichog.
Data for several marine invertebrates are summarized in Tables 6-5
and 6-6. Toxicity values for these benthic organisms were in the range
of 25 mg/1 to 700 mg/1, the most sensitive being the hermit crab (Pagurus
Ion gi carpus) . The data for these invertebrates show that in almost
every instance there was a marked and progressive decline in LC values
between 24 and 168 hours (Eisler and Hennecky 1977). Toxicity levels
for all the organisms tested were confined to a relatively narrow
range.
In studies of marine organisms used as human food products it was
found that Pacific Coho Salmon ( Onchorhynrhus kisutch) contained three
times the concentration of nickel than that found in other fish tested,
and twice the level found in mollusks. Lobsters were found to contain
higher levels of nickel than several mammalian species tested (MAS 1975).
6.1.4 Factors Affecting Toxicity
The effects of water hardness on the toxicity of nickel, primarily
n freshwater systems where hardness values can vary substantially,
was previously discussed. Other factors that affect nickel toxicity
are not as well studied. Eisler (1977) studied the effects of mixed
metal solutions (Mi, Mn, Zn, Pb , Cu, Cd) on a marine bivalve mollusk
(Mya arenaria) . It was found that these clams showed increasing resistance
to metals with decreasing ambient water temperature. Marine bivalves
6-9
-------
TABLE 6-5. ACUTE TOXICITY OF NICKEL - ESTUARINE
MACRO INYERTEB RATES
Organism Tine Intarval (hr) (LC5Q tng/1)
Source: Eisler and Henneckv (1977).
Starfish 24 270
Asterias forbesi 96 150
168 13
Mucisnail 24 540
Nassarius obsoletus 96 72
168 16
Sandworn 24 320
Nereis virens 96 25
168 25
Hermit crab 24 130
Pagurus longicarpus 96 47
168 30
Softshell clam 24 700
Mva arenaria 96 320
168 112
6-10
-------
TABLE 5-6. TOXICITY OF NICKEL SULFATE - MARINE
MACROINVERTEBRATES
Organism
Prawn
Shrinip
Cockle
Crab
Ovster
Hours
48
48
48
48
48
LC50
(mg/1)
13.9
125
7500
255
100-150
Source: U.S. EPA (no date)
6-11
-------
are known to exhibit consistent and measurable changes in content of
selected netals (including nickel) with increasing growth, changing
seasons, and as a reflection of the metal content of the sediment sub-
strate and sediment interstitial waters (Eisler 1977). In studies
with rainbow trout, however, it was found that temperature did not
affect toxicity of nickel (Hughes et al. 1979).
6.1.5 Conclusions
According to the literature surveyed, the lowest concentration of
nickel at which effects have been observed in aquatic organisms is
0.1 mg/1, which caused reduced growth in algae. Levels above 1 mg/1
begin to cause acutely toxic effects to a variety of aquatic organisms,
including freshwater fish and zooplankton, and to several aquatic insects.
Data for marine organisms are not extensive, but that which is available
shows that salt water biota, both fish and invertebrates, are less sen-
sitive to nickel than are freshwater organisms. Sublethal effects on
development of carp eggs and embryos also occur at concentrations
greater than 10 mg/1. The most resistant organisms tested were several
benthic marine invertebrates, including clams, mussels, and oysters,
in which mortality levels were in the range of 100 rag/1 to 900 mg/1.
The most sensitive marine organism tested was the Atlantic Silverside,
of
Water hardness, as measured by CaC03 content, has a considerable
effect on solubility and toxicity of nickel. This probably accounts
in part for the apparent greater toxicity of nickel to freshwater
biota than to marine organisms. This relationship must be kept in
nind when examining toxicity data for a substance such as nickel, but
unfortunately information on water hardness under experimental condi-
tions is often not given in the literature. Information on the relation-
ship between other water quality parameters and toxicity of nickel was
unavailable.
In summary, general concentration ranges can be established at
which certain effects of nickel are seen in the laboratory. These
ranges are not rigidly defined, however, and may overlap as a result
of differences among species, life stages, or environmental variables.
• 0.0054 -0.086 mg/1 Background levels of nickel in fres'rwater
and salt water.
• 0,10 -0.020 g/1 Represents the detection limit in one survey '
for nickel in water with total dissolved solids
(TDS) of 200 vg/1 and 400 Ug/1, respectively,
(see Chapter 3.0 - Materials Balance).
• _
-------
1.0 - 10 ng/1
10 - 100 mg/1
100 - 1000 mg/1
co 0.73 mg/1, but did noc affect growth and
survival of adults. Reduced growth in 4 algae
species at 0.1-0.7 mg/1. Background levels
of nickel in many fresh and salt water environ-
ments also found in this range. Several river
basins, particularly the Ohio, but including
the Lower Mississippi, Lake Erie, Missouri,
Western Gulf, and Tennessee River, reported
annual average nickel concentrations
greater than 100 ug/1 for two or more years
of the 10-year period of STORE! data.
This range includes the threshold of acute
toxic effects in soft water (low CaC03 con-
tent) for several species including freshwater
zooplankton (cladocera, copepods), fathead
minnow, guppy, rock bass, bluegill, striped
bass, and several aquatic insects. Values
in this range occurred as maximum ambient
levels on infrequent occasions, but in several
river Basins , including the Ohio (4 years),
Tennessee (3 years), Upper Mississippi (3 years),
Lake Michigan (2 years), Missouri (2 years),
Lower Mississippi (4 years), and the Western
Gulf (2 years), there were higher levels.
Acutely toxic values for numerous organisms,
including Atlantic Silverside, winter flounder,
Channel catfish, Killifish, trout, purapkinseed
sunfish, copepods, and aquatic insects, are
in this range; caused carp eggs not to under-
go embryonic development. Lethal at 24 and
96 hours to several benthic marine invertebrates,
including mudsnail, hermit crab, and sandworm.
In hard water, toxic levels occur at the upper
end of this range.
Toxic at 96 hours to several marine organisms,
including starfish, softshell clam, and Muirani-
chog. No freshwater toxicity values found in
this range. Levels in this range were reported
only twice, in the North Atlantic Region and
the Missouri River. "So exposure data for salt
water was available.
6.2 EXPOSURE
5.2.1 Introduction
Nickel, the 24th most abundant element in the earth's crust, is
present in surface and groundwaters as a result of weathering of minerals
containing the element. Aquatic organisms are exposed to low-level
6-13
-------
natural background concentrations of nickel in freshwater and salt
water environments in the range of 0.0054 mg/1 to 0.086 -ng/1 (U.S.
EPA 1980b) , as well as to anthropogenic sources of nickel.
In an aqueous environment, nickel exists infrequently in the insoluble
elemental form. The nore common fom is the free, divalent nickel ion
(Xi"1"") which results fron one of the nickel salts or one of the many
organonickel compounds or complexes. As a trace metal, nickel is
believed to be an essential element to living organisms, but the extent
to which this is true is unknown. Nickel compounds are generally very
soluble in distilled water, with solubility decreasing with increasing
CaC03 content (hardness).
In the water column, nickel, like many of the other trace metals,
is concentrated in the colloidal portions of the dissolved solids. Com-
pared to other substances found in water (e.g., course particulates)
the colloids can carry a tremendous amount of metal. Therefore, if a
stream or water body contains sufficient colloids, it can transport
considerable quantities of a metal which otherwise has a low solubility.
In sediments, it is believed that nickel is sorbed onto particles
and is in a form which is neither exchangeable nor readily soluble in
alkaline waters, thus not available to biota (Perhac 1974).
6.2.2 Mpni 13 r in g Data
This section discusses the notantial for exposure or aquatic organ-
isms to nickel in water bodies in the United States
Among the major sources of nickel emissions to the aquatic environ-
ment are secondary scrap raetal processing, electroplating, smelting
and refining, and battery production. Discharges to land, a small
portion of which may eventually reach water via runoff or leaching,
result from electroplating and mining and milling. For the most part,
nickel wastes from these industries are discharged to tailing ponds,
sludge lagoons, landfills, or open dumps, and not directly to surface
waters. Dischargers from these industries are discussed more fully
in Chapter 3.0 - Materials Balance.
Mean nickel concentrations in 1980 for 16 major U.S. river basins
are given in Table 4.1 (Chapter 4.0 - Environmental Pathways). These ranged
from 3 ug/i for the western Gulf of Mexico to 31 ug/1 for the Ohio
River. A fe:« reports are available which studied nickel levels found
in sediments and surface waters of various water bodies. Levels of
nickel detected in water supplies of the 100 largest U.S. cities (1962)
are cited in the National Academy of Sciences study on nickel (NAS 1975).
These ranged from 0.6 ;i2/l to 25 Lg/1. Nickel levels found in marine
and freshwater environments and in sediments in the Pacific Northwest
and other locations in various parts of the world are referenced in
Laevastu and Thomuson (1951).
6-14
-------
Nickel content of sediment was determined for two different types
of streams in Tennessee (Perhac 1974). One, the Tennessee River, is
located partially in an urbanized area and flows over a mineralized
streanbed; the other, Joe Mill Creek, is located in a rural non-mineralized
area. Sample data for these streams are provided in Section 4.5 - Monitoring
Data. In general, the levels of nickel in Tennessee River sediments were
substantially higher than those in Joe Mill Creek.
Nickel concentrations were also measured in surface waters and
sediments of various Adirondack lakes. Nickel ranges found were 0.4 ug/1
to 14.3 ug/i for surface waters 0.2 ug/g to 5 ug/g for surface sedi-
ments, and O.i ug/g to 2.9 ug/g for subsurface sediment (10-20 cm).
For this report, the STORE! data base for the 10-year period 1970-
79 was examined to ascertain aquatic exposure levels of nickel (U.S.
EPA 1980b), The data revealed that the majority of nickel concentrations
found in surface water from 18 reporting major river basins are in the
low-to-mid -jg/1 range (1-500 ug/1 or less). A summary of these data
by year and river basin is presented in Table 6-7.
The maximum concentration found was one occurrence of 800 mg/1 in
1974 in the North Atlantic Region. The distribution of percentages of
observations over the entire concentration range measured are presented
in Table 4-1. Over the 10-year period examined, there were numerous
observations of low concentration in the range of 1-50 mg/1. During
this period there were approximately 50 incidences of concentrations
rantjins from 1 mg/1 to higher amounts. This range includes threshold
levels for acute and chronic toxic effects to several aquatic organisms ,
including zooplankton, insects, and some fish, in soft water (see Section
6.1). River basins reporting levels greater than 1 mg/1 included the
North Atlantic, Tennessee, Ohio, Missouri, South Central Lower Mississippi,
Lake Erie, and Lake Michigan. During some portion of the 10-year period,
nearly all of the river basins reported values in the range known to
cause reduced growth in freshwater algae (100-900 ug/1).
6.2.3 Conclusions
Beginning in 1972, there was a steady increase in the number of
occurences of concentrations greater than 1 mg/1, with 1974 having
the most reported concentrations in this range (see Table 6.7). From
1974-1979, the data for the Ohio River Basin consistently showed maximum
concentrations in the 1-50 mg/1 range. In addition, for all of the
ranges of nickel values reported, there was a marked increase in the
percentage of observations in the higher ranges (low-to-mid ug/1) over
the 10-year period for all river basins. No information on the temporal
persistence, areal extent, or precise source of any of the higher con-
centrations for any of the river basins reporting was available, nor
was any other water quality information available, particularly CaC03
content, which would help in determining the availability of the nickel
to biota. However, despite occasional levels in the low mg/1 range and
6-15
-------
TAIil.K 6-7. STOKKT MON1TOUTNC DATA SHMMAKY
(all values Jn MR/1 except where noted)
Year
1970 01;l
max 450. UK/ 1
min 10
im>stb . 20-40
1971 01
cr.
^ max 180 ut;/l
cr.
min 0
most <9()
1972 01
max 1 30
min 0
most 10-100
1973 01
••ax 1250
min 0
River Basin
02
270
0
< too
02
5 1 00
0
<100
02
690
0
< 100
03
45
0
06
500
50
50-100
03
20
20
20
03
14
0
<10
04
920
1.0
07
340
1.2
<60
04
1000
0
.1-100
04
510
0
<50
05
480
0
08
63
0
<10
05
140
0
<70
05
20000
1650
0
<100
06
630
0
09
21
0
<20
06
130
0
<100
06
110.
.02
<80
07
1020
1200
0
10
300
100
100
07
1000
0
200-1000
07
300.
0
< 1 00
08
25
0
12
100
10
100
08
1400
0
<100"
08
300
0
<10
09
1 28001
1080-
9
13
45
6
12-45
<45
09
110
0
<,00
09
510
.01
10-500
10
|5 100
0
21
6
1
<6
10
230
30
<230
10
1160).
1910)
0
<100;
100-
1000
12
720
0
22
10
0
10
13
100
< 1 00
1 1
130
75
75,
130
14
400
10
14 21 22
120 38 14
10 0 11
< 1 00 0 * 1 4
12 13 14 17 22
9200 20 178 10 93
II Jl/A/l £-\t I/O IU / J
5000
20 ]() 5 10 93
<200 <2() < 100 10
22
17
11
<.4 10-1000 < 100 25-700 <10()
-------
TAIH.K 6-/. STOHKT MON1TOIUNC DATA SUMMAIUKS (CONT1NIIKI))
(all values in p^/1 except, wliero noted)
1974
max
in i n
IIIUH l
1975
max
ON
1
*~| in 1 n
must
1976
II1.IX
01
70
0
< 10.
01
150
0
10-100
01
220
02
8mg/l
0
< 100
02
320
1
1-100
02
5 SO
03 ' 04
250 26°°
1400
0 5
<50 10-1000
03 04
23 100
0 5
<10 1-100
03 04
52 100
05
1600
1225
0
10-
800
05
1300
0
10-430
05
1200(2)
06
07
13* «<«
0
10-
900
06
210
0
10-
100
06
100
.02
10-
400
07
620
0
10-
100
07
2700
08 09
1120 ug/lj
170 210 mg/lj1
0 8
< 70 10-
900
08 09
140 650
0 0
2-100 2-100
08 09
350 500 1-
10 12
9240 680
0 0
10- 10-700
900
10 II
510 400
0 0
10-
100 <100
10 11
12 mg/1 120
14
450
3
10-450
12
720
20
1 00-
700
12
1.7 lug/I
15
12
12
12
13
37
_
—
13
80
21 22
24 150
1 1.0
< 24 «.'jO
14 21 22
400 8 4'j
10 .0 1.0
10-100 <10 <4'j
14 21 22
1 80 8(> 30
21
11
(14values)
in i n
IIIOS t
1977
max
m in
must
0
<100
01
100
0
<100
0
1-500
02 01
230 320
1 0
0 3.4
1-50 3-100
04 05
1200 975
3.4 .02
100-300 100- 100-
-------
TABLE 6-7. STOKKT MONITOR fM DATA SUMMARIES (CONTINUED)
(all values In pg/1 except where noted)
o>
M
Co
Year
1978 01
900
max
1
in ! it
100-900
"">st 10-100
1979 01
max 280
ni in 0
most <2HO
02 03 04 05 06
540 700 190 31 mg/1 2800
00300
100-700 1.19-
<100 <1()0 <100 31.2mg/l <100
(117
values),
<100
02 03 04 05 06
190 200 440 31.7mg/l 100
0 0 0 0 <1()
10-100 <100 <100 *j°~ <]OQ
rag/l(141)
10-900
ug/1
07
300
0
<100
07
400
0
10-
400
08
110
0
<80
08
260
2
10-
100
09 10 11
1 mg/1 200 140
0 0 0
100-
1000(32)<200 <100
1.-100
09 10 1 1
900 220 260
0 0 0
'900 10~100 * lo()
2-100
12 13 14
505 500 450
0 1 1
100-500
1-100 <45 10-450
12 13 14 15
150 50 80 100
00 00
<60 <50 <80 <10
15
250
0
<25
19 21
200 25
100 0
100- <|0
200
22
20
0
<10
These numbers are River Das in Codes. See Appendix K for list of codes and name.
The "must" category represents an estimation of the range(s) in which a majority of the
values for that river basin occurred.
Source: U.S. EPA (1980b)
-------
many in the range 100-500 ug/1, which has been found to cause chronic
effecrs in algae and freshwater fish eggs, overall the levels of nickel
found in streams are below 100 •jg/l. No adverse effects to aquatic
organises have been found below this level. An exception to this gen-
eralization is the Ohio River Basin, which for several years showed
niaxiaun nickel concentrations in the low-to-raid Tig/I range, and con-
sistently reported many values in the 100-900 pg/1 range.
6.3 SUMMARY
The range of concentration levels at which nickel has been found
to cause chronic and acute toxic effects to aquatic biota is quite
broad, less than 1 sag/1 to greater than 1000 ms;/l. Water quality
considerations, CaC03 content in particular, and the chemical form of
nickel present have a significant effect on the toxicity levels ob-
served. In general, however, the threshold of toxic effects to
most fish and invertebrates is in the range of 1-10 mg/1.
Concentrations at or above this range are of concern to aquatic
systems. The STORE! data base for the 10-year period 1970-1979 reported
approximately 50 observations of nickel levels greater than 1 ng/1
in the entire United States. These were distributed over several river
basins and not concentrated in any one area. In addition, there were
several observations of nickel in the range of 100-500 ug/1, levels which
have been found to cause chronic effects to algae and freshwater fish
eggs. Although the Ohio River Basin reported maximum levels in the
100-900 -jg/1 range over the 10-year period, the number of these obser-
vations was not frequent enough to be of .concern. Overall in the
United States the levels of nickel reported in streams is below 100
ug/1, so that aquatic biota would not be considered to be exposed to
harmful concentrations of nickel.
6-19
-------
REFERENCES
Baudan, X.F.; Scoppa, P. Bull. Environ. Contain. Toxicol. 12:745;
191'-. (As cited in Friedrich and Filice 1976)
Biesinger, K.E.; Christensen, G.M. Effects of various metals on survival,
growth, reproduction, and metabolism of Daphnia magna. J. Fish Res.
Board Can. 29:1691; 1972.
Blaylock, B.C.; Frank, M.L. A comparison of the toxicity of nickel to
the developing eggs and larvae of carp (Cyprinus carvio). Bull. Environ.
Contam. Toxicol. 21:604; 1979.
Brown, V.M.; Dalton, R.A. The acute lethal toxicity to rainbow trout
of mixtures of copper, phenol, zinc, and nickel. J. Fish Biol. 2:211;
1970. (As cited in U.S. EPA 1980a)
Buikema, A.L. et al. Evaluation of Philodina acuticornis (Rotifera)
as a bioassay organism for heavy metals. Water Resour. Bull. Am. Water
Resour. Assoc. 10:648; 1974. (As cited in U.S. EPA 1980a).
Eisler, R. Acute toxicities of selected heavy metals to the softshell
clam, Mya arenaria^. Bull. Environ. Contain. Toxicol. 17:137-145; 1977.
Eisler. R.; Kennecky, R.J. Acute toxicities of Cd2+, Hg+~, Cr , Ni~' ,
and Zn*-+ to estuarine macrofauna. Arch. Environ. Contam. Toxicol. 6:
315-323; 1977.
Friedrich, A.R. ; Filice, F.P. Update and accumulation of the nickel ion
by Mytilus edulls. Bull. Environ. Toxicol. 16(6):750-755; 1976.
Hughes, G.M.; Perry, S.F. ; Brown, V.M. A morphometric study of effects
of nickel, chromium, and cadmium on the secondary lamellae of rainbow
trout gills. Water Res. 13:665-679; 1979.
Hutchinson, T.C. Comparative studies of the toxicity of heavy metals
to phytoplankton and their synergistic interaction. Water Pollut. Res.
(Canada). 8:63; 1973. (As cited in U.S. EPA 1980a)
Hutchinson, T.C.; Collins, F.W. Effect of H+ ion activity and Ca-+ on
the toxicity of metals in the environment. Environ. Health Persp. 25:
47-52; 1978.
Hutchinson, T.C.; Stokes, P.M. Heavy metal toxicity and algal bioassavs.
ASTM STP J73, Am. Soc. Test Mater, p". 320; 1975. (As cited in U.S. EPA
1980a)
Laevastu, T.; Thompson, T.G. The determination and occurrence of nickel
in sea x^ater, marine organisms, and sediments. J. Consert. 21:125-143;
1951.
Lind, D. et^ al. Regional copper-nickel study. Aquatic toxicology study.
Minnesota Environmental Quality Board, State of Minnesota. No date.
6-20
-------
National Academy cf Sciences (XA3). Nickel. Washington, DC: National
Academy of Sciences; 1975.
Perhac, R. Water transport of heavy metals in solution and by different
sizes of particulate solids. Knoxville, TN: Tennessee university Water
Resources Research Center. Research Report No. 32; 1974. Available
from XTIS; Springfield, VA; P3232 427.
Pickering, Q.H. Chronic toxicity of nickel to the fathead minnow. J.
WPCF 46:760-765; 1974.
Pickering, Q.H. ; Henderson, C. The acute toxicity of some heavy inetals
to different species of warm water fishes. Air Water Pollut. Int. J.
10:453; 1966. (As cited in U.S. EPA 1980a}
Rehwoldt, R. et aj.^ Acute toxicity of copper, nickel, and zinc ions tc
some Hudson River fish species. Bull. Environ. Contam. Toxicol. 6:445;
1971. (As cited in U.S. EPA I980a)
i
Rehwoldt, R. at_ al_. The acute toxicity of some heavy metal ions toward
benthic organisms. Bull. Environ. Contam. Toxicol. 10:291; 1973
(As cited in U.S. EPA 1980a)
Rehwoldt, R. , e_t al. The effect of increased temperature upon the acute
toxicity of some heavy metal ions. Bull. Environ. Contam. Toxicol. 8:91;
1972 (As cited in U.S. EPA 1980a)
Schweiger, G. The toxic action of heavy metal salts on fish and
organisms which fish feed. Arch. Fischwiss 8:54; 1957. (As cited
in Warnick and Bell 1969)
U.S. Environmental Protection Agency (U.S. EPA). Ambient water quality
criteria for nickel. Washington, DC: Office of Water Planning and
Regulation, U.S. Environmental Protection Agency; 1980a.
U.S. Environmental Protection Agency (U.S. EPA). MDSD priority
pollutant file. Nickel. Washington, DC: Monitoring and Data
Support Division, U.S. Environmental Protection Agency; no date.
U.S. Environmental Protection Agency (U.S. EPA). STORET. Washington,
DC: Monitoring Data and Support Division, U.S. Environmental Protection
Agency; 1980b.
Warnick, S.L.; Bell, H.L. The acute toxicity of some heavy metals to
different species of aquatic insects. JWPCF 41(2)-.280-284'; 1969.
Willford, W.A. Toxicity of 22 therapeutic compounds to fishes. Bur.
Sport Fish Wildl. Resour. Publ. 35. Washington, DC: U.S. Department
of the Interior; 1966.
6-21
-------
-------
7.0 RISK CONSIDERATIONS
This chapter evaluates the human and non-human risk associated
wich exposure to nickel based on available data on effects and known
exposure levels in the environment that were documented in chapters
5.0 and 6.0.
7.1 HUMAN RISK
The risk of adverse human effects due to exposure to background
levels or nickel through ingestion, inhalation, and percutaneous expo-
sure has not been found to be particularly great. Certain nickel
compounds, however, are potentially toxic at elevated doses and/or
as a result of routes of exposure which enable the compounds to
accumulate at high concentrations at the cellular or subcellular
levels of the body. An important factor in considering the risk
of nickel toxicity is adequate assessment of whether or not nickel
can reach the susceptible sites in the organism. Ingested nickel is
believed to have low toxicity because it is poorly absorbed. As a
result high levels of nickel in the diet of experimental animals are
tolerated with minimal effects.
The najor area of concern is nickel exposure through inhalation
which has been shown, in certain circumstances, to cause toxicity.
Exposure to nickel through inhalation is probably most prevalent in the
industrial occupational setting. The animal studies evaluated in Chapter
5.0 indicate that nickel carbonyl and nickel subsulfide are carcinogenic.
Other adverse effects identified in the animal studies were:
• nickel carbonyl was teratogenic and fetotoxic and
• high levels of nickel in drinking water or diet had
adverse effects in neonates.
Finally, an observed human effect reported in the literature indicated
that nickel contact dermatitis occurs but is not fatal.
Considering these human effects and identifiable routes of exposure,
human risk is addressed in the context of four exposure scenarios:
ingestion of drinking water, inhalation of ambient air, inhalation of
cigarette smoke, and percutaneous exposure. In addition a brief review
of occupational exposure data was made.
7.1.1 Ingestion of^ Drinking Kater
The lox^est dosage of nickel found in animal studies to cause
adverse effects was 443 ug Ni/kg body weight/day. Nickel is found in
drinking '.waters and in foods of the average diet. Drinking waters
typically contained nickel at around 10 ug/1, although concentrations
were occasionally higher (50 ue/1 to 75 ug/1). At these levels and
considering an average daily water consumption of 2 liters, drinking
7-1
-------
water is a minor constituent (less than 15£) of the average dietary in-
take cf nickel—100 -jg to 900 ug. This dietary intake corresponds to
a daily dose of 1.4 to 12.9 us nickel/kg body weight/day, which is far
below the adverse effects level of 443 ug nickl/kg body weight/day.
Neither nickel in drinking water nor that contained in dietary
foods can be considered a human health risk due to the low levels
found in the environment and the fact that nickel is poorly absorbed
or rapidly excreted from the body.
7.1.2 Inhalation of Ambient Air
The primary route of exposure to nickel which has been shown to
cause adverse health effects is the inhalation route. In the animal
studies the most common effects of exposure to nickel carbonyl and
nickel subsulfide were the occurrence of respiratory tract cancers
and neoplasms of the lung.
Considering an exposure scenario in which humans inhale ambient
air, levels of "nickel" in the air and the associated speciation of
nickel must be identified. In ambient air, it is unlikely that
nickel carbonyl (Ni(CO>4) will persist for any significant length of time
due to the unstable nature of Ni(CO>4. It is more probable that in the
case of ambient air exposure, nickel subsulfide 011382) will occur as the
compound causing adverse effects; by its physical-chemical nature, ^382
is more likely to persist in the atmosphere, particularly in the vicinity
of combustion sources.
Concentrations of nickel in ambient air have been reported for
urban, non-urban, and industrial locations. In the urban and non-urban
environment, "nickel" concentrations are lox^ (0.6 to 690 ug/m3); if all
of the reported "nickel" were nickel subsulfide, risks associated with
this exposure could be evaluated. However, speciation of the reported
nickel concentrations in air has not been reported, consequently a
statement of risk cannot be made. Sampling of industralized urban
areas would provide more reliable data on actual concentrations in
the air and associated nickel speciation. Such information would
allow for a more complete evaluation of risk of exposure to ambient
air.
7.1.3 Inhalation of Cigarette Smoke
Stahly (1973) reported that cigarette smoke may contain 3 ug nickel
carbonyl per liter of smoke. The smoking conditions were 36-ml puffs and
approximately 14 puffs per cigarette, or ^500 ml of smoke per cigarette,
which contains about 1.5 pg of nickel carbonyl. These measurements are
somewhat theoretical and need to be confirmed. Moreover, the respiratory
retention of nickel carbonyl during smoking is not known. If one assumes
these measurements are accurate and if retention is taken to be about
66?o, then each cigarette contributes about 1 -_g nickel carbonyl in absorbed
dose. From Table 5-10, an equivalent one-pack-a-day lifetime smoker
7-2
-------
(^2 packs/day for 35 years) is predicted to be at an excess lifetime
per capita risk of 0.05 to 0.1;= due to the nickel carbonyl alone.
According to Che Surgeon General's report (U.S. DHEU 1979), lung
cancer is the number one cause of death due to malignancy, and
cigarette smokers are at u? to 20 times the risk of non-smokers of
dying of lung cancer. It is estimated that there are 390,000 deaths
frota all cancer in che United States yearly, including 92,400 from
lung cancer. In 1976, the estimated age-adjusted mortality rate due
to lung cancer was 63/100,000/year for males and about 19/100,000/year
for females.
The actual contribution of nickel carbonyl in cigarette smoke to
the incidence of lung cancer and cancers at other sites in the body
can not readily be estimated; however, the prediction from Table 5-10
is not totally unrealistic. For example, the lifetime probability of
death due to cancer from the above data is estimated to be about 13%
(390,000 x 70/215 x 106) and of cancer of the lung, about 3%. Of the
13% or 3%, the predicted contribution from an equivalent lifetime
one-pack-a-day smoking habit (0.05-0.1%) is a small fraction.
7.1.4 Inhalation in the OccupationalEnvironment
Occupational exposure to nickel compounds via inhalation was con-
sidered in this risk assessment primarily as a. means to put waterborne
and dietary exposure in perspective. Occupational exposure to nickel
carbonyl and nickel subsulfide is most likely to occur in the ferrous
metals (iron and steel), electroplating, and nickel refining industries.
It is in these environments that nickel carbonyl and subsulfide are
both likely to occur, and likely to persist long enough to allow expo-
sure at levels sufficient to cause adverse human effects. A cursory
review of occupational exposure data indicated that data on speciation
of nickel were not available; all nickel reported in occupational
data was in the "general" form. Consequently, it was not possible
to evaluate exposure to or risk associated with these compounds in
the occupational environment, although it is probable that exposure
occurs. Neither compound is found in the aquatic environment or in
food, thus there is no exposure via ingestion of drinking water or in
the diet.
7.1.5 Nickel Con tact Dermatit is
A number of studies summarized in the NAS report (1975) indicate
that patients with dermatitis frequently react to nickel patch tests
(between 6 and 152). Unanswered, however, is the incidence of nickel
sensitivity in the general population, and, more importantly, what is
the capacity of nickel, in the variety of ways that the general population
is exposed, to act as a skin sensitizer.
The most frequently reported causes of nickel allergy are from
jewelry (especially earrings) and clothing fasteners. Typically,
7-3
-------
women have a much higher incidence of nickel sensitivity than men.
Interestingly, so-called "hypoallergenic" posts for pierced earrings,
manufactured for people who apparently have developed allergies to the
1^-karat gold posts, contain nickel. The ability of stainless steel
kitchen appliances and cookware to sensitize persons to nickel is
unknown.
7.1.6 Conclusions
The risk associated with exposure to nickel is primarily confined
to inhalation of cigarette smoke and possibly ambient air if most
of "nickel" in ambient air is in the form of nickel subsulfide. The
risk associated with inhalation of nickel carbonyl in cigarette smoke
is only a small fraction of the risk associated with the other com-
ponents of cigarette smoke; in the case of nickel carbonyl an excess
lifetime per-capita risk is estimated at 0.05 to 0.1%. The risk
of exposure to nickel subsulfide in ambient air cannot be evaluated
until further sampling and analysis of nickel speciation is performed
in the industrial and urban environments. Similarly risk associated
with exposure to nickel carbonyl or subsulfide in the occupational
environment cannot be evaluated without further data. Dermatitis
caused by contact with nickel-bearing objects is not fully understood
but is not considered a life-threatening problem. There is no iden-
tifiable risk associated with ineestion of nickel in drinking water
and the diet.
7.2 NON-HUMAN RISK
Nickel is occasionally found in surface freshwaters at concentra-
tions (total) exceeding the lowest effects levels (dissolved) reported
for aquatic organisms. Additionally, the criteria to protect fresh-
water aquatic life at a 24-hour average and maximum concentration (set
for soft waters) are violated or almost exceeded by maxiraun surface
water concentrations on numerous occasions, most notably in the soft
waters of the North Atlantic major river basin. Under certain circum-
stances, nickel occurs in concentrations in surface waters at levels
sufficiently high to potentially cause adverse effects in aquatic
species,based on information developed under laboratory conditions.
Little field data regarding nickel toxicity in natural systems are
available to confirm this hypothesis. Mean surface water concentra-
tions rarely exceed these criteria.
7.2.1 Exposure
In order to ascertain the potential risk of aquatic organisms in
relation to nickel, it is necessary to compare effects levels to expo-
sure levels. In the case of nickel, as for other metals, this is
difficult because adverse effects levels are determined for dissolved
nickel salts and exposure concentrations report total nickel. Nickel
is highly soluble at neutral pH in soft waters; however, nickel in
-------
watar is commonly associated with suspended solids and sediment,
reducing its biological availability. Only a fraction of the nickel
concentration typically reported in monitoring data is biologically
available, making the "actual" concentration (in terms of availability)
lower than the reported level. This increases the gap between effects and
exposure levels. Unfortunately, determining this fraction on a national
scale is not possible due to its dependence on pH, hardness, concentra-
tions of suspended solids and complexing agents, and other factors some
of which vary independently. A site-specific analysis is required for
this type of interpretation of total nickel concentrations.
As a worst case assumption, all of the nickel reported in total
concentration measurements can be considered available. As discussed
in Chapter 5.0, typical surface water concentrations over the past 10
years were below 0.5 rag/1. In 1970 the mean concentrations in 16
river basins ranged from 0.003-0.03 aig/1. On occasion, concentrations
vere reported between 0.5-50 mg/1. The maximum reported concentration
was 800 rag/I.
7.2.2 Aquatic_Ef^fe^cts and Rj.sk Considerations
Chronic effects levels are commonly reported for fish living
in soft freshwater at greater than 2 mg/1. Invertebrates are more
sensitive, with the lowest observed effects level at 0.5 mg/1. Salt-
water species, according to the limited data available, are less
sensitive than freshwater species. These effects are discussed more
fully in Chapter 6.0.
Table 7-1 presents the effects and exposure concentrations for
comparison, Nickel concentrations in surface water are typically
below effects concentrations; this is also true for most sensitive
species. Only certain algae species may be affected at typical
ranges of nickel concentration. However, the high exposure concen-
tration range, such as is associated with rare observations in the
Ohio River Basin most recently (1978, 1979) and others in the past, is
equivalent to the concentration range causing acute effects in most
freshwater species. Assuming total availability on these occasions
of high nickel concentrations, aquatic species are at risk of deleter-
ious effects in certain river basins for short periods of time. How-
ever, as discussed previously, the assumption of total availability
is an unreasonable one. To better define the risk, a netal speciation
model using local system parameters (e.g. pH, etc.) must be implemented
to calculate available nickel concentrations. Salt water concentrations
were not available so it was not possible to evaluate the risk of
marine populations in regard to nickel.
7«2.3 Sensitive Species
The aquatic species reported to be most sensitive to nickel con-
centrations in water according to the available data are listed in
Table 7-2. It is interesting to note, however, that the range of
-------
effects levels for most freshwater species is a narrow one of approxi-
mately one order of magnitude. Therefore, the difference between the
levels at which adverse effects are experienced by the most sensitive
species and those experienced by other species is not very extreme.
7.2.4 Regipna1 Areas of Higher Risk
The major river basins in which a number of nickel concentrations
were higher than the mean included the North Atlantic, Tennessee, Ohio,
Missouri, S. Central Lower Mississippi, Lake Erie, and Lake Michigan.
The highest reported nickel level was in the North Atlantic. These
observations were infrequent and, therefore, are not believed to be
typical nickel concentrations for these major river basins.
/ -o
-------
TABLE 7-1. COMPAKISON OF REPORTED EFFECTS AND
EXPOSURE LEVELS TOR AQUATIC ORGANISMS
EXPOSW100 mg/I
as CaCO-j)
Most Sensitive
Species
27
3.8
al)uta from STORET Water Quality System retrieved on July 22, 1980; discussed in Chapter 6.0 in wliic
total nickel concentrations given.
Applies to acute and chronic effects; dissolved nickel concentrations given.
.Not enough data were available to differentiate between sensitive and typical species.
For Stickleback, in estuarine species, in nickel nitrate.
[Concentration does not consider water hardness.
For nickel sulfate.
-------
TABLE 7-2. SPECIES SENSITIVE TO NICKEL
CONCENTRATIONS IN WATERa
Freshwater Fish
Estuarine Fish
Marine Fish
Freshwater Invertebrates
Salt Water Invertebrates
Algae
Fathead minnow (Pimphales promelas) ,
goldfish (Carassius auratus), guppy
(Lebistes reticulacus) and bluegill
(Lepomis macrochirus).
Stickleback
Atlantic silversides
Daphia (Daohia aiagna, D. pulicaria and
DA hyalina) and rotifer (?hi.lo.dina
acuticornus)
Sandworm (Nereis virens) and Hertait
crab (Pa^urus longicarpus)
Scenedesinus acuminata
All data discussed in Chapter 6.0,
-------
REFERENCES
National Academy of Sciences (MAS). Xickel. Washington, DC: National
Academy of Sciences; 1975.
SCahly, E.E. Some consideration of metal carbonyls in tobacco smoke.
Chern. Ind. (London) 13:620-623; 1973.
U.S. Department of Health, Education, and Welfare (U.S. DREW). Smoking
and Health; a report to the Surgeon General. DREW Publication No. (PHS)
79-50066. Washington, DC: U.S. Department of Health, Education, and
Welfare; 1979.
-------
-------
APPENDIX A
MOTE 1; Hanna mines garnierite
and several associated minerals which occur in altered periodotite.
The ore, which averages 1.2% nickel, is removed with power shovels
and trucks; blasting is not a common practice (Matthews, 1979). The
ore is screened at the mine and either sent directly to the tramway
surge pile or to the crusher and all boulders are rejected. Efforts
to blend the ore into a uniform feed for the melting furnaces begin
at the mine and continue throughout all subsequent operations.
Once the ore is crushed, the material is visually classified
(the intensity of the green color of garnierite is directly
proportional to the nickel content [Boldt, 1967]) and directed to
the ore product or reject stockpile. From the product stockpile,
the materials are calcined and preheated either in a rotary kiln or
a multihearth furnace. The ore is next melted in either an electric
or a melting furnace and poured into reaction ladles where reduction
by addition of crushed ferrosilicon occurs. Coke, lime, and iron
ore are also added to produce the end product—ferronickel.
NOTE 2: The first settling pond received about 12,500 liters
of process water per minute (l-tnin."^) of which 9,800 l-min"^
were returned to the process. Approximately 1,500 l-min'1 were
lost by evapotranspiration and underflow to a nearby creek. Thus,
overflow to the second pond amounted to nearly 1,200 l-min'^. The
second pond also received mine site runoff water whose volume ranged
widely throughout the year, (i.e., zero for approximately six months
and as high as 2.2 million liters per day during the rainy season).
Though the second pond had no surface discharge during the dry
season, inputs balanced by evaporation and an undermined subsurface
flow to a nearby creek, significant discharges did occur during the
rainy season. Average discharge over the year amounted to 455,000
liters per day with a mean nickel concentration of 0.03 mg/1.
Therefore, approximately 5 kilograms of nickel were discharged from
the second holding pond based on a year-round operation. (The
concentration of nickel in the wastewaters was determined by
analyses of samples collected from the second settling pond and was
comparable to values obtained by company personnel (0.038 mg Ni/1 of
wastewater).
NOTE3; Production a- AMAX Nickel Refinery was impaired during
the last four months of 1979 by a work stoppage (Sibley, 1980).
NOTE 4: Based on 1980 nationwide particulate emissions from
steel manufacture, and assuming similar quantities of particulates
A-l
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were emitted in 1979, and 750 ppm nickel (or 750 g Ni/kkg
particulates) :
Particulate Nickel
Furnace Types Quantity (kkg) Enicted (kkg)
Open Hearth Furnace 27,573 21
Basic Oxygen Furnace 19,501 15
Electric Arc Furnace 21,768 16
Total 37 kkg
NOTE 5: Based on production figures from Sibley (1980) and
wastewater discharge data from secondary copper snelters/refiners
(EPA, I979a; Table 3.4), ic is known that: total amount of
copper-base scrap processed in 1979 = 3,240 kkg (100%); amount of
that total fron new scrap =• 2,800 kkg (or 86%); amount from old
scrap » 440 kkg (or 14%), then 867, and 14* of total waste steamed
fron processing of new and old copper-base scrap, respectively.
A total of 565 kkg and 92 kkg of nickel wastes were generated
from refining of new and old copper-base scrap, respectively. Of
the 32 known secondary copper smelter/refiners, 20 have no
discharge; 7 are direct dischargers, 5 are indirect dischargers
(EPA, I979a). Assuming that the total discharge is divided equally
among the remaining 12 plants, then 327 metric tons and 237 kkg of
nickel were discharged to surface and POTW sinks, respectively from
plants processing new copper-base scrap. Likewise 53 kkg and 38 kkg
of nickel were discharged to surface and POTW sinks, respectively by
plants processing old copper-base scrap.
NOTE 6: Less than 1 kkg of nickel is assumed to be produced
based on the following data: (1) Few plants practice coproduct
nickel recovery; (2) those that do recover coproduct nickel have
efficient systems because the nost widely used evaporators are
closed systems so that aerosols are recycled; (3) discharges from
centrifuges are recycled to electrolytic cells; and (4) slitnes are
processed for metal recovery (see Figure C.3, Appendix C; EPA,
I975c; and Outokumpu Engineering Inc., 1980).
NOTE 7; Negligible is defined here as <1 kkg; 754,082,000 kkg
of distillate fuel were consumed in 1979 in the U.S.; one liter of
distillate fuel weighs approximately 845g or 0.000845 kkg (EPA,
1977a), therefore 8.9 x 1011 liters of distillate fuel were
consumed for that year. If the average nickel concentration of
4-75 Ug/nl determined from 17 distillate fuel oil number 2 samples
(Lee and Duffield, 1979) represents a typical nickel concentration
for distillate fuels, then approximately 4 kkg of nickel were
contained within all the distillate fuel consumed. Taking into
A-2
-------
account control device efficiencies, tae quantity 01 nickel emitted
to the atmosphere would most likely be <1 kkg.
Low concentrations of nickel have oeen reported to be
associated with automobile exhausts. This nickel most likely
results from ablation rather than combustion of fuel because: (1)
very small quantities of nickel have been identified in fuels, (2)
the exhausts tested came from automobiles equipped with
nickel-containing reduction catalysts and (3) the rate of nickel
emission decreased rapidly with mileage accumulation (Lee and
Dnffield, 1979).
NOTE8; Based on Hamilton Standard electroplating data base,
of the total 443 electroplating facilities whose effluents contained
nickel, the average flow rate » 22,700 liters per hour and the
average nickel concentration » 3.4 ag/'l. Based on a 365 day/yr
operation and 16 hr/day, then O.i5 kkg/yr/plant was discharged.
Nearly 75% of electroplating facilities discharged to POTWs; the
remaining 252 discharged to rivers or basins. Given that 200 kkg
nickel discharged as effluent represented 5% of the total wasteload,
approximately 3,800 kkg of nickel were disposed of in sludge
annually (based on average nickel removal efficiencies of 95% at
electroplating facilities, Patterson, 1976; i-iasarik, 1980;.
Approximately 90% of electroplaters release sludges to public or
private landfills; tne remainder is claimed off site. Thus, 3,040
kkg of nickel were disposed to land in 1979.
NOTE 9: In 1977 more nickel sulfate was produced than any
other nickel compound. Assuming 1979 production figures to be
comparable to 1977 values and based on tne manufacturing process
(i.e., filtration sludges were reprocessed and treatment tank
liquors recycled, EPA 1977o), engineering judgments indicate that
approximately 3 kkg of nickel were released to land and water,
each. Nickel concentrations in wastewater sludges from woven fabric
and dying facilities averaged 32 mg/1. Assuming wet sludge to be
952 water by weight and the total sludge output to oe 28,000 kkg/yr,
then 1 kkg of nickel contained in sludge was disposed to land.
NOTE 10; Based on EPA estimates (1975a and 1976),
approximately 1,470 kkg of nickel were used in battery manufacture
in 1979. Based on EPA questionnaire surveys (1973b), 4 kg of nickel
were emitted to the atmosphere per kkg of nickel processed. Of the
10 battery facilities, 8 were direct and 2 were indirect
dischargers. Based on EPA effluent discnarge rates (after
treatment), 15 kg Ni/kKg batteries produced and a total production
of 890 kkg by the 2 indirect dischargers, 13 kkg of nickel were sent
to POTWs. Tne 8 remaining plants discnarged 0.01 kg Ni/kkg
batteries produced (production of 3,560 kkg batteries), therefore
less than 1 kkg was discharged to waterways directly.
A-3
-------
Based on 1.7 kg Ni in sludge from wastewater treatment at Che 2
indirect plants/kkg batteries produced, and a total production of
890 kkg batteries. Therefore 2 kkg of Ni were discharged to land as
sludge. Two of 10 plants disposed of scrap cells to land. Based on
an EPA discharge race of 1.5 kg Ni/kkg batteries produced and a
total production of 890 metric tons, 1 kkg of Ni was disposed to
land as scrap.
NOTE 11: The nickel content of sea water ranges from
0.1-0.5 \lg/l (NAS, 1975). Therefore, with an enrichment factor of
200 and a total aerosol production from sea salt sprays of 10^ kkg
annually (Nriagu, 1979), approximately 40 kkg of nickel were
aerosolized from this source in 1979.
NOTE 12: Nriagu (1979) estimated world-wide nickel emission
from volcanic activity to range from 2,400 to 56,000 kkg annually
with a value of 3,SOO kkg being most likely.
NOTE 13: Aerosol formation from forest fires has recently been
discussed by Young and Jan (1977) wno measured dry deposition rates
of nickel in tne area covered by a forest fire smoke plume. Nickel
deposition fluxes ranged from 0.01 Co 0.13 yg/m^/day and averaged
about 0-07 pg/m^/day during the fire; postfire values of nickel
deposition flux is approximately 0.01pg/m^/day. Based on tnese
data, aerial nickel fallout to a 10,000 km? area was estimated to
be 120 kg/day and 33 kg/day fron fire and nonfire sources,
respectively. Aerosol nickel is removed eventually from the
atmosphere by dry deposition and/or washout, although the rates of
removal are unavailable.
NOTE 14: Significant amouncs of nickel may be released to Che
atmosphere from vegetation. The most likely manner in which plants
exudate nickel is that nickel associated with particles of various
sizes is released from Che plane surfaces during rapid growth and/or
transpiration. It is possible chac epicucicular waxes are the
nickel carriers and Chat fragmentation and loss of wax rodlets occur
during rapid leaf expansion. AlternaCiveiy, there may oe a
mechanism which involves Che production of airborne salt crystals
generated by diffusiophoresis associated with water loss during
rapid CranspiraCion. Assuming vegetation exudaCes Co approximate 75
x 10° kkg annually, an average ash concent of 11%, and nickel
concentration in asn residue to be 25 g/g then 200 kkg were emitted
from this source. (Goldsmith and May, 1965; Beauford and Barber,
1977.)
NOTE 15: Nickel, as referrea to here, means nickel contained
within an alloy; generally .£50%.
A-4
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NOTE 16: Old nickel-based scrap contains varying percentages
of nickel (and impurities) and is processed at many different plants
whose recovery efficiencies and disposal practices vary. Also, the
flow of this scrap is difficult to follow due to the numoer of
different groups who handle secondary scrap (see Figure C-4,
Appendix C).
NOTE 17: The annual unit flow rate of water from waste
electrolyte (electrolytic refining area cleaning water) was 31.9 x
10^ 1/yr. The nickel concentrations in treated and untreated
wastewatera were 310,000 and 3,100,000 yg/1, respectively;
therefore 9.8 and 98.3 kkg of nickel were contained in the total
volume of treated and untreated waters from one plant,
respectively. Six secondary copper refineries practiced treatment
and six did not. Therefore, 6(9.8 kkg) + 6(98-3 kkg) of nickel, or
(58.3 kkg) + (592.8 kkg) - 651.6 kkg was released to water.
Furthermore, 6(98.8 - 9.8) = 534 kkg of nickel were removed during
treatment and disposed to land, i.e.:
534 kkg removed and disposed to land
592.8 kkg in *
untreated waters
from 6 plants treatment 58.8 kkg sent to water *•*
that treat
ana
-652 kkg
592.8 kkg in
untreated waters ^
from 6 plants discharged water]
that do not treat ^«—
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NOTE 21: Fuel oils are broadly classified into two major
types: distillate and residual. Distillate oils (fuel oil grades
1, 2, and 4) are used mainly for residential and commercial
applications where easy fuel burning is required. Distillate fuels
not only are more volatile and less viscous than residual oils
(whicn require preheating to be pumped) but also are cleaner and
contain negligible ash (see Appendix B, Note 7). Residual oils
(fuel oil grades 5 and 6) are used mainly in utility, industrial,
and large commercial applications. Because residual oils are
produced from the residue after the lighter fractions (i.e.,
gasoline, kerosene, and distillate oils) have been distilled from
crude oil, significant quantities of ash are often present.
NOTE 22: Flue gas cleaning equipment is generally employed
only on large oil-fired boilers. Mechanical collectors are
primarily useful in controlling particulates generated during soot
blowing, upset conditions, or when a very dirty, heavy oil is
fired. During these situations, high efficiency cyclonic collectors
can control up to 85 percent of the particulates, Dut when a clean
oil is combusted, they will not be as effective. Electrostatic
precipitators are commonly found in power plants tnat at one time
fired coal. Precipitators that were designed for coal flyasn
provide only 40 to 60 percent control of oil-fired particulate,
while 90 percent collection efficiencies have been reported for new
or rebuilt devices specifically designed for oil-firing units.
ScruDbing systems have been installed on oil-fired boilers, to
control particulate. These systems can achieve particulate control
efficiencies of 50 to 60 percent (EPA, 1977a).
NOTE 23: The major asbestos mineral used commercially,
chrysotile (Mg^OHjoSi^iQ), generally contains 1.5-1-8 mg
nickel/g of chrysotile as an isoinorphic substitution for magnesium
(Streib, 1978). Dusts from milling of asbestos could release small
quantities of nickel, as a component of chrysotile, to the
atmosphere; moreover tailings from milling operations are dry piled,
providing a possible route for nickel discharge to either the
atmosphere via wind erosion or aquatic environments via leaching.
According to EPA plant trip data, an asbestos mill producing
36,300 kkg/year and using a baghouse collection system emits 0.18
kkg asbestos/yr (Wood, 1980). Assuming this emission rate to be
similar for all of the five U.S. asbestos mills which produced
93,300 metric tons asbestos in 1979 (Clifton, 1980) with a maximum
nickel content of 1.8 mg/g in chrysotile, less than 1 kkg of nickel
was directly emitted to the atmospnere.
Possibly a more significant source of nickel release to the
environment from asbestos production is the dry piling of waste
tailings. Because recovery of asbestos fiber from ore is low (i.e.,
A-6
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5% Co 50".), a significant aoount of chrysolite remains in che waste
(Streib, 1978). Further, because chrysolite reacts with acids,
weatnering of waste tailings may release significant amounts of
nickel to "he environment. The magnitude of this source, however,
is unknown.
NQTS 24: Otner methods of electroplating wastewater treatment
are reverse osmosis, evaporation, ion exchange, and electrodialysis.
NOTE 25: Nickel azo yellow (Colour Index number 12775), a 2:1
nickel complex of a bidentate oj-hydroxyazo ligand, is used for its
green-yellow color in PVC and other vinyl plastics, particularly
where light stability is important (e.g., automobile parts). Nickel
antimony titanate is formed by high temperature fusion ( <1000'C) of
nickel ancimonate and titanium oxide in dry form. The pigment is
extremely insoluble as the nickel antimonate takes position in the
titanium oxide lattice structure. Though the amount of pigment
contained per liter of paint depends on the particular color, yellow
paint averages 22-360 g/1. Nickel dimethylglyoxime, a red pigment,
is not commercially produced in significant quantities.
NOTE 26: Hydrotreating is an oil refining process using a
cobalt-molybdenum catalyst to reduce the sulfur and nitrogen content
of crude oil (Miller, 1979). Smaller amounts of nickel-molybdenum
catalysts are used for hydrotreating as well. Cobalt is in short
supply however, and increased use of nickel-containing catalysts is
being encouraged. Nickel catalysts are superior to cobalt catalysts
in terms of nitrogen removal, but do require higher operating
pressures.
NOTE27: A framework for calculating the total nickel flow
through the nation's POTWs (see Table C-17 in Appendix C) is
provided by data from a recent EPA study. A material balance of
nickel at tne treatment plants can be constructed using a total POTW
flow of approximately ID** I/day (E?A, 1978c) and median values of
180 g Ni/1 (influent) and 107 g Ni/1 (effluent). It is assumed
for purposes of these calculations that influent and effluent flow
rates are equal, i.e., that water loss from sludge removal and
evaporation is small compared to influent flows. It is further
assumed that while nickel is recycled witnin the activated sludge
process, all will eventually be wasted. Thus, the value for nickel
in sludge is simply the difference between the influent and effluent
nickel totals, as there is an assumed negligible loss of nickel to
the air. Using the assumptions, 2,660 kkg of nickel were disposed
as sludge to land from POTWs in 1979 and approximately 3,900 kkg of
nickel were discharged to water from POTW effluent streams. An
alternative method for estimating the annual nickel release to
sludge is as follows: the quantity of dry sludge produced in 1979
was 6 x 10° kkg; assuming the nickel concentration of POTW wet
A-7
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sludge Co be 8 ag/i where wet sludge is 95% water by weight,
approximately 960 kkg would have been discharged to land (EPA,
1979d) . Approximately 257. of all municipal sludge is landfilled,
257, spread on land, 15% ocean dumped, and 35% incinerated (EPA,
1979c).
NOTE28; Baaed on soil studies, nickel solubility (like most
other heavy metals) increases with soil pH. Within the pH range of
4-8, organic matter in soils forms nickel complexes which
effectively preclude further migration or plant uptake (Antonsen and
Springer, 1968).
A-8
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APPENDIX 3
This distribution of nickel emissions and discharges from
combustion of coal and oil* for energy production is derived from the
following basic assumptions.
(1) The ash present in coal is distributed between bottom ash,
flyash collected, and particulate stack emissions (i.e., ash
loss via slagging is negligible); and
(2) the distribution of the nickel originally present in the feed
material is dependent only upon particle size.
Thus: Ash in (A ^ = Ash out (A Q t) = Afa + A + A , or
1 « Ain » Ab + Ac + Ae
where Afa - Fraction Bottom ash
Ac = Fraction Flyash collected
Ae = Fraction Flyash emitted, also,
AC + Ae = Af where Af » Fraction of ash that is total flyash.
The amount of ash which appears as bottom ash, is dependent upon
fuel and boiler type. For boilers which fire pulverized coal (1Q cm), approximately twenty-five percent appears as flyash.
*Though the derivation is applicable to gas fired boilers as well,
natural gas contains negligible amounts of nickel and thus is an
insignificant source of nickel emissions to the environment (Slater
and Hall, 1977).
B-l
-------
Essentially all of the ash present in residual oil appears as flyash.
The amount of flyasn collected in turn depends upon the particulate
control device used, (either singlely or in combination), which
generally are cyclonic devices, electrostatic precipitators and
baghouses. The fraction of ash emitted as flyash, control device
efficiency, application of control, effective efficiency, fine
particulate fraction, atmospheric emission fraction, and land
dispersion fraction are shown in Table B-l. For pulverized coal-fired
boilers, ash emission fractions are calculated as follows:
(1-A.) = A = 0.20
T D
A - (A,}E - 0.71
C !
Ae = (AJ(I-E) = 0.088
The fraction of the ash emitted to the atmosphere (A ) is further
Subdivided into particulate which remains suspended (A <3 urn) and
that which eventually settles to land (A >3 u^) in the following way:
A2>3u - AePf = 0.057
Ae<3y = Ae(l-Pf) = 0.031
Nickel emissions and discharges within a boiler are a function of
particle size, nickel concentration increasing with decreasing
particle size. Nickel concentration of flyash by particle size ranges
is shown in Table B-2. Using these data (and assuming the nickel
concentration of bottom ash and collected flyash to be equal) relative
nickel concentrations of bottom ash (C.), collected flyash (C ) flyash
emitted > 3n (C < 3w), and flyash emitted <3u (C >3u) are calculated
B-2
-------
to be 1.0, 1.0, 3.9, 1C. 5, respectively. Nickel emission factors are
calculated in the following way.
!b c """
where
fu = Fraction of nickel contained in bottom ash
fc * Fraction of nickel contained in collected flyash
fe<3u = Fraction of nickel emitted as participate <3u
f >3y = Fraction of nickel emittea as participate natter >3u-
These fractions are calculated using ash emission fractions and
relative nickel concentrations:
Ni = A. • CK •*• A • C + (A , »C , ^ + (A . .C , )
total D b c c v e<3M e<3M' ; e>3M e>3MJ
A - C
f _ c c
c Ni . .
total
A C
f <3um = e<3ym ( e<3gm)
e -N1
^total
A (C
^
'"total
Consequently, nickel emission factors by boiler type and media
are shown in Table B-3.
B-3
-------
Table 0-1. Mass Efficiency of ('articulate Collection on Utility Boilers'
Fuel Boiler
Type
Coal Pulverized
Cyc 1 one
Stoker
Oil All
Gas All
CO
1
Fraction of Control
Ash Emitted Device
As Flyash Efficiency
(AF)
0.8
0.50
0.25
1.0
1.0
0.92
0.91
0.80
0.50
0
Application Effective Fine Particulate
of Controld - - Ef.f-ici-«!aL_ Fraction (<3 KB)
Calculated Reported /n ,
(E) (Pf}
0.97 0.89 0.89
0.71 0.65 0.88
0.87 0.70 0.65
0.20 0.10 0.10
0 0
0.35
0.52
0.14
0.90
0.90
Atmospheric Emissioir Land Dispersion
(<3 H») (>3 I'm) Hyash' B~6ttom As'h
Ac < 3 CRi Ae ->3 cm
0.031
0.031
0.012
0.8!
0.90
0.057 0.71 0.20
0.029 0.44 0.50
0.075 0.16 0.75
0.19
Om ._
a) Data were obtained from utilities accounting for one-half of the total U.S. utility consumption of coal in 1974.
l>) Engineering estimates based upon published data.
c) Fraction collected of the total particulate mass entering control devices. Data includes both test results and reported design efficiencies.
d) Fraction of utility boiler equipped with particulate control devices.
e) Effective efficiency equals control device efficiency multiplied by application of control.
f) Slater and Hall, 1977.
(j) Fine partkulate fraction is the fraction of total particulate mass emission <3 pm, derived from particulate size distribution entering
control device; the effective mass efficiency; and the effective fine particulate efficiency.
h) Fraction emitted based upon reported effective efficiency, fine particulate fraction, and distribution of coal ash between flyash and bottom
ash. For pulverized and cyclone boilers, the distribution fraction between flyash and bottom ash (engineering estimates based upon unpublished
data) is estimated to be 0.8 and 0.2 respectively; for stoker fired boilers, the distribution fraction between flyash and bottom ash is estimated
to be 0.2 and 0.8 respectively.
Source: Slater and Hall, 1977.
-------
rable 3-2. Nickel Concentration In Coal Flyash as a Function of Particle Size
Particle
Diameter
vVm)
Flyash retained in the plant
Sieved fraction:
>74
44-74
Aerodynam'cally sized fractions
>4C
3C-40
20-30
15-20
10-15
5-10
*5
Airborne flyash
>11.3
7.3-11.3
4.7-7.3
3.3-4.7
2.1-3.3
1.1-2.1
Nickel
Concentration
//g/g
100
140
300
130
160
20C
210
230
260
460
400
440
540
900
1600
Mass
Fraction
(:i)
66
22
2
3
3
0
0
0
0
.30
.39
.50
.54
.25
.80
.31
.33
.08
Source: Natusc.h, et al., 1974.
An equal mass distribution among particular size fractions is assumed.
B-5
-------
Table B-3. Nickel Emission Factors by Boiler Type and Media
Fuel Boiler Type Nickel
Bottom Ash Flyash
Captured
(fb) (fc)
™ Coal Pulverized 0.4 . 0.49
tn
Cyclone 0.36 0.32
Stoker 0.56 0.12
Oil All — - — -
Distribution
Flyash
Emitted (<3um)
/f 0 m)
* e< 3 pro
0.22
0.24
0.10
0.96
Flyash
Emitted (>3,ym)
(f o )
v e >3 pm '
0.15
0.08
0.22
0.04
*"
Fraction emitted based upon ash distribution and relative nickel concentration of flyash <3/j, flyash >3j/, flyash
collected, and bottom ash. The concentration ratios are (see Table A-3 also):
= 10.5
flyash emitted (
flyash emitted (>3/v) = 3.9
flyash collected = 1.0
bottom ash = 1-0
-------
APPENDIX C
Tabls C-l. Physical Properties of Nickel
Atomic number 28.
Electronic configuration
Atomic weight 58.71
Melting point °C 1453
Specific gravity at 20°C 8.908
Crystal structure face-centered cubic
Lattice constant at 24.3°C,A 3,5168
Thermal expansion coefficient at
0-100°C, per °C 13-3x10
Specific heat at 200°C, cal/g 0.1225
Latent heat of fusion, cal/g 73.8
Thermal conductivity, cal/(sec)(cm)
(C°/cm) 9 100aC 0.198
300°C (99.94% purity) 0.152
500°C 0.148
Electrical resistivity at 20°C ohn-cm 6.844
Magnetic transformation temperature, °C 357
Boiling point, °C (by extrapolation of
vapor pressure data 2730
Reflectivity, %
9 0.30 (ultraviolet) 41
IP 0.55 (yellow-green) 64
3 3.0 (infrared) 87
Source: After Nlcholls, 1973 and Adamec and Kihloren, 1968.
C-l
-------
Table C-2. Solubility Products of Various Nickel Salts
Salts u^O y_=0.1 (unless otherwise noted
Ni(OH)2 (fresh) 14.7 14.3
(aged) 17.2 16.8
N12[Fe(CN)6] 14.9&
NiC03 8.2b
Ni3(As04)2 25.5b
NiS^ 18.5
N1S8 24.0
NiSv 25.7
Source: Ringbom, 1963.
Jtost values refer to a temperature of 20 or 25°C
Ionic strength varied and was not specified.
C-2
-------
Table C-3. Nickel-Containing Minerals
Mineral
Si! icate and Oxide
garnierite2
nickel ferrous
limonite
Sul fides
pentlandite
mUlerite
heazlewoodite
pclydymite
violarfte
siegem'te
bravoite
Arsenides
ni ceo lite
maucherite
rarmelsbergite
gersdorffite
chloanthite
Antimoride
breithauptite
Arsenate
annabergite
Formula
(Ni,.Mg)6Sid01Q(OH)g
(Fe,Ni)0(OH)-nH20
(Ni,Fe)9S8
NiS
Ni3S2
Ni3S4
N12FeSd
(CC,Ni)3S4
(N'i,Fe)S2
NiAs
NinAs8
NiAs2
NiAsS
(NiAs2)
NiSb
NVs208.SH20
Nickel Content, 1.
up to 47.0
low but variable
34.22
64.67
73.30
57.86
38.94
28.89
24.0
43.92
51.85
28.15
35.42
32.53
29.4
Garnierite is a generic term applied to a series of mixtures of
hydrous nickel -magnesium silicates. Several nickel silicates,
each an analog of a magnesium mineral (given in brackets) can occur
as constituents of garnierite:
nimite, (Ni .Mg.Fe.Al J(Si ,A1 )0
[chlorfte].
willenseite, (Ni ,Mg)3Si4010(OH)4 [talc];
pecoraite, N13Si205(OH)4 [clinochrysotile] ;
nepouite (N1 ,Mg)35i205(OH)4 [Hzardite]; and
pimelite, (Ni ,Mg)3Si40lfj(OH)2- 4HgO [Stevensite]
(Faust, 1966; Faust, et_ aj_. , 1969; De Waal, 1970).
C-3
-------
Table C-4. Nickel in Water from Major U.S. River Basins'
River Basin Mean Nickel Frequency of
Concentration, ^g/Hterb Detection, %
Northwest
North Atlantic
Southeast
Tennessee River
Ohio River
Lake Erie
Upper Mississippi
Western Great Lakes
Missouri River
Southwest-Lower Mississippi
Colorado River
Western Gulf
Pacific Northwest
California
Great Basin
Alaska
8
8
4
4
31
56
15
10
5
17
12
3
10
10
4
5
22.0
28.1
20.9
8.8
25.2
53.2
15.2
9.1
2.0
9.7
8.0
2.1
10.5
13.8
15.8
11.1
Source: Koop and Kroner, 1970.
aThe detection limit for nickel in water with total dissolved solids
(IDS) of 400^g/l was 20//g/l; if IDS amounted to 200 //g/1, the
detection limit would be 10
Only occurrences of nickel were used in calculating the mean.
C-4
-------
Table C-5. Relative Rates of Aerosol Production Mechanisms
MECHANISMS RELATIVE RATE
Sea-to-Air Transport of Salts 100
Natural 3as-to-Particle Conversion 74
Wind Blown Dust 50
Anthropogenic Gas-to-Particle Conversion 38
Anthropogenic Particles 10
Volcanoes 4
Forest Fires 3
Meteoretic Debris 1
Source: Mulvey, 1979 .
C-5
-------
Table C-6. Source and Composition of Mattes Imported into the U.S., 1979
Source
iNew Caledonian
South Africa0
(Reoublic of)
Botswana
Australia
Average Composition (%}
Ni
75
40
40
75
Cu
0
40
40
0
CO
1.5
0.5
0.5
1.5
S
(b)
16
16. Od
(b)
Fe
(b)
0.2
0.2d
(b)
Source: Hoppe, 1977, unless otherwise noted.
3A11 imported matte is processed at AMAX Nicki
Metal Climax, Incorporated, Braithwaite, Louisiana.
aAll imported matte is processed at AMAX Nickel Division of American
The remainder of the matte is sulphur and iron.
cReceived in powdered form; similar in composition to the Botswana
matte (Sibley, 1980), ...
Similar in composition to the New Caledonian matte (Sibley, 1980).
C-6
-------
Taals C-7. N1ck«T Wastes: Energy Production, ;S79 (k.kg)
Ssjrst
Coal
Situr.iccus
Anthracite
'.Ignite
Petroleum
Residual
Bisfillate
Este**na] Combustion
Coa' ; total)
Bituminous (total)
'ulverizes 3ry
'uNsrizee wet
Cyclar.e
All stokers
Anthracite {total •
'ulve'ized dry
?u"verizec net
Cyclone
All steers
Lignite ;tst*i;
Pi;lver'zec ary
».j!v*rijee -et
Cyclone
All stokers
P-trale-jr;
Sesioual oil
•ConcuStlon tjrtine
St«ais generation
ConiBlntd cycle
C-istillate oil
Ccmoustior, turoine
Steam generation
Ceniinea cycle
SPACE -EATING AND Q7HES
Coal1
tncustry
?es-dertis-/Csn-e-:lal
Coke plants
Petroleum
aesicual oil
InCuStry
Ses i de" t i a 1 .'Ccife'c 1 a 1
"ransocrtaticr.
Distillate oil
Industry
Resident?; I/ Comers la'.
Trans:or-.ition
:=H
917
530
34
909
154
754
479
442
336
42
53
a
3J
12
2
IS
1
77
7;
71
5
3
1
122
6C
S
70
913
32
61
21
746
30
139
479
,50C
.733
,354
.300
.500
.032
.500
.733
477
,733
,123
«=;
949
• ••-
949
,354
,367
,«S
.21"
,03:
.350
,230
33
.310
328
,532
.430
.434
667
,::c
nn[
,OCO
,000
,300
,400
,:oo
neg
.300
,SOC
,000
,ooc
,50C
»or'
,303
,30C
.000
.003
.000
,000
,OOC
.000
,000
,000
.000
,000
noo
.000
,000
.coc
,coc
.000
,000
.0:0
.300
.coc
.600
,000
,50C
.000
,300
,300
,500
,coo
.000
,;oc
,000
.00:
.COG
.300
,occ
.COG
.ooc
•*/• f*
t jUu
.3CC
Nickel2
S.30C
S.1QC
100
unknown
7.700
ne?
S.3CO
6,200
4,700
600
740
120
47
47
100
37
7
55
3
3,620
3.523
4
3300
16
negh
negh
J
1.930
34Q
110
gao
4,100
4.100
3.100
neg
1,000
nejh
1 „•
J
~S~,i',
2.23C
2.240
1,740
22C
240
40
15
!5
30
1C
3
17
1
3,620
3,620
4
3,600
16
ntgh
neg
620
270
40
310
4,100
4,100
3. ICO
neg
1,000
neg '
h
neg
EN
• — —
neg'
1.380
1,350
i.::c
130
130
10
5
5
24
3
z
13
<1
3.48C
3.43C
4
3.460
15
19C
80
10
103
3.940
3.940
2.93C
96C
__
» 2...-
Mfl
890
710
50
60
30
10
10
id
5
1
4
'1
140
140
<1
140
1
433
190
20
220
160
16C
12-
40
TAL RELEASES
-drcw
nege
4,990 '
4.37C
3.670
470
56C
17C
40
40
20
30
S
4C
- J
14C
14C
4
140
I
negh
neg"
1 . 740
750
100
sac
160
160
120
neg
40
h
neg
n.;h
-cter
6"'
, :,5s
neo
nee
neg
neg
neg
neg
ne;
neg
neo
C-7
-------
Table C-7. (concluded)
^Production and consumption data are from Monthly Energy Review published by National Reliability Council, Princeton, N.J. and are rounded to nearest
thousand metric ton. Data niay not add due to rounding.
Nickel concentration by coal type is assumed to be: Bituminous coal - 14 mg/k<|; Anthracite - 50 mg/kfj; Lignite - 3 mg/kg (see Appendix B);
also see Appendix A. note 7.
cThe amount of nickel emitted to the atmosphere was calculated as follows:
3fim=amount of nickel associated with particles greater than 3pm
in diameter and that were initially emitted to the atmosphere.
but eventually settled to land
eNation emission burden from coal storage piles is estimated to be 630 kkg/yr; Dlackwood and Machter (1978). Nickel fugitive emissions are calculated
using the following nickel concentrations: Bituminous coal - 14 mg/kg; Anthracite - 50 mg/kg; Lignite - 3 mg/kg.
Acid mine drainage is reported to average 0.72 ing/1 (range: 0.01 to 5.59 my/1) at an average flow of 3.8x10 liters per mine-day. Drainage from
5673 coal mines is considered in this calculation.
^Screening sampling data for the electric power operating point source category: the average flow from an ash pond is reported to be 21.7x10 I/day-
plant. Nickel concentration is reported to be 0.05 mg/1. Assuming each of the 379 steam electric plants identified to have an ash pond.
*See Appendix A, note 7, for details.
'Coal combustion exclusive of utilities is assumed to be in stoker fired boilers.
-------
Table C-8. U.S. Fossil Fuel Consumption by User in 1979
o
I
ID
USER
Electric Utilities
Industry3
Coke Ovens
Residential /Commercial
Transportation
TOTAL
Coal (106 kkg)
480
60
70
8
618
%
78
10
11
1
100
Refined Petroleum Product (106 1)
83,315
211,788
200,220
564,132
1,059,894
%
8
20
19
53
100
Source: Monthly Energy Review, U.S. Department of Energy, 1980.
Excluding coke ovens.
-------
Tdhle C-9. Sources of Nickel Contained in Sludoe from Select Industrial Processes
PROCESS/WASTE
Ferrous Metal Sine) tiny and Refining
Iron and steel coke production
Iron arid steel production
Annum i a still 1 i me s 1 ud
-------
Table C-10. Nickel Wastes from Cement Plants in Metric Tons (kkg), 1979
, -
Process
Dry kilns
Dryers,
Grinders
Total
Wet kilns
o Dryers ,
^ Grinders
Total
Cement Producted Emission
103 kkga Factor (kg/kkg)b
30,000 122
48
70
41,600 114
16
130
Total Particulates
103 kkgc
3,660
1,440
5,100
4,700
665
5,400
' Environmental Releases (kkg)
Air
143
56
199
182
28
210
Water6
neg
neg
neg
neg
neg
neg
Land
1 ,872
737
2,609
2,404
340
2,762
aTotal quantity of cement produced in 1979 was about 71.6 x 10 kkg; assuming 58% of production used wet
method and 422 used the dry method (as was the case in 1976, Minerals Yearbook, 1976).
Emission factors expressed as kg of particulate emitted without control devices per ton of cement produced
(EPA, AP-42, Part B).
GThe product of emission factor and cement produced.
•Assuming all cement plants have control devices; control device population equally distributed among multi-
cyclones, electrostatic precipitators (ESPs), ESPs and multicyclones, and fabric filter units with 80, 95,
97.5, and 99.8% particulate removal efficiencies which when averaged equals 93%; number expressed is quan-
tity of particulate matter emitted to atmosphere. Nickel concentrations in particulate matter emitted from
cement plants after control devices range from 100-1,000 ppm (Lee and Duffield, 1979), and a mid-range
value is used.
ec.
f
Significant levels of nickel have not been detected in wastewaters from cement manufacture; i.e., mean
values for nickel waste loadings were reported as zero, EPA, 1973c.
Particulate matter removed by control devices with average efficiency of 93% (see footnote d).
-------
Table C-T1. Nicks! Concentrations in Select Industrial Wastewaters
Industry
Meat Processing
Fat Rendering
Fish Processing
Bakery
Miscellaneous Foods
Brewery
Soft Drinks and
Flavoring Syrups
Ice Cream
Textile Dyeing
Fur Dressing and
Dyeing
Miscellaneous
Chemicals
Laundry
Car Wash
Firms
Sampled
16
4
1
3
4
2
3
i
22
6
10
4
39
NO. Of
Samples
53
16
4
8
16
43
12
3
65
28
23
14
39
Average Concentration
mg/1
0.07
0.028
0.14
0.43
0.11
0.04
0.22
0.11
0.25
0.74
0.10
0.10
0.19
Source: Klein et al., 1975-
C-12
-------
~ac"s C-!2.
in ,'arisjs Plants arc
Vegetable or F>uit
Concentration, ppei
Wee Weight:
Potato, raw
peas, fresh, 'rojen
9eas, canned
Peas, split, cried
Beans, string, frozen
Seans, string, canned
Beans, navy, cries
3eans, yellow-eye, dried
Seans, 'ec icicrey, dried
Spinach, fresh
C2"ery, fresh
Beet greens
Swiss chard, organic
Escarjle, fresh
Chicory, 'rash
Lettjce, garden, organic
Lettuce, head
-------
Table C-13. Nickel Allovs: Percent Comoosition and Use
Components
Alloy
Use/Properties
nickel
nickel and iron
90-99.5
0.5-10
anodes
wroucht alloy
electroplating
transportation and
steels
wrought high-
strength steels
including
maraging
0.5-20 structural and
high-strength
cast alloy
steels
1-6 alToy cast
and steels
14-36
30-90 magnetic alloys
14-23 permanent
magnet alloys
and magnetic
compensator
alloys
4-90 nonmagnetic
alloys
5-40 coated and clad
metals
22-50 thermal expan-
sion and
thermoelastic
alloys
earth-moving equip-
ment; heavy machinery;
low-temperature
applications.
hull plate; missile
casings; machinery;
forming dies.
heavy machinery; rail-
road; steel mill rolls;
cryogenic applications.
heavy machinery; machine
tools; automotive and
diesel engines; brake
drums; corrosion resis-
tance; abrasion
resistance
communications; elec-
trical equipment.
motor, generator, radio,
and instrument parts.
electrical and magnetic
equipment parts.
petroleum, chemical,
and food-processing
equipment
chronometer springs;
electronic, instrument
parts.
C-14
-------
Table C-13. (Continued)
nickel and copper 2-13
10-30
25
over 50
5-30
1-15
45
high-copper
alToys
cupronickels
coinage alloy
high-nickel
alloys
nickel silvers
(Ni-Cu-Zu)
nickel brasses
and bronzes
electrical
resistance
alloy
instrument and control
parts
tubes and plates in
condensers and heat
exchangers
coinage
corrosion resistance;
strength; chemical,
petroleum, and food-
processing equipment.
flatware; hollow ware;
electrical equipment
telephone equipment;
jewelry; zippers;
plumbing fixtures;
architectural trim
spring applications;
bearings; valves;
pumps .
resistance elements;
thermocouples.
nickel and chromium i-on
(iron base and w
nickel base) , oc
iL-O3
10-80
6-20
electrical heating elements
resistance alloys
heat-resisting
alloys
superalloys
stainless steels
high-temperature
applications
gas turbine and jet
engine
corrosion resistance;
strength; chemical,
petroleum, and food-
processing equipment
others
0.5-98 age-hardenable
alloys
98 composite
94-98 nickel-manganese
alloys
corrosion resistance;
strength
high-temperature
applications
spark plugs; ignition
tubes.
C-15
-------
Table C-13. (Concluded!
55-65
85
nickel-moly-
bdenum-iron
and nickel-
molybdenum-
chromiurn-iron
alloys
nickel-si 1 icon
alloys
corrosion resistance;
strength
corrosion resistance;
hardness alloys
nickel and aluminum 2
1-2.5
1
cylinder head
and piston
alloys
low-expansion
alloys
bearing alloys
automotive and aircraft
parts
automotive and air-
craft parts
automotive and air-
craft parts
Source: Adamec and Kihloren, 1968.
C-16
-------
Table C-14. Composition of Mickel Plating Baths
o
I
TYPE OF BATH
Watts bath
Hard bath
Chloride
Chloride sulfate
Sulfamate
Sulfamate chloride
COMPOSITION
N1S04.6H20
NiCl0.6ILO
2 2
II3B03
NiS046H20
NH4C1
ILBO-j
3 3
NiCl9.6H90
2 2
H3B03
N1S0..6IU)
4 2
NiCl0.6ILO
2 2
H.,BO.,
3 3
Ni(NH2S03)2
H3B03
Ni(NH2S03)2
N1C10.6H00
2 2
H3B03
CONCENTRATION (g/1)
330
45
38
180
25
30
300
38
200
175
40
450
30
300
6
30
Source: Lowenheim, 1979,
-------
Table C-15. Wastewater Characteristics of Electroplating Shops
o
I
00
Plant
A
I)
C
0
E
F
G
II
I
J
K
L
M
N
0
P
Q
R
S
T
U
V
W
Flow Rate (gph)a
800
5000
3800
11700
3700
8400
2100
2500
7500
3400
44000
11500
27000
500
360
22300
41000
3300
76800
1900
49200
15000
13700
Nickel Content(mg/l)b
0.6
1.0
0.2
0.4
1.0
0.5
1.7
1.9
2.0
0.1
1.0
1.4
2.0
0.1
2.7
4.7
0.5
0.5
0.4
3.0
0.1
0.8
0.3
DISPOSAL
Municipal
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
X
Surface
X
X
X
X
X
X
Source: EPA, 1979b.
— ~. A «. . - _ .» A- 1 f\f\ •» ^
. Flowrates rounded to nearest 100 gallons per hour.
Ni content rounded to nearest tenth.
-------
Table C-16. Nickel Chemicals and Applications
Chemical
Application
Nickel Sulfate NiS04
Nickel Chloride N1C12
Nickel Carbonyl Ni(CO)4
Nickel Oxides NiO
Nickel Cyanide N1(CN)2
Nickel Hydroxide Ni(OH)2
Raney Nickel NiAl3
Nickel Antimony Titanate
Electroplating baths, fungicides
Electroplating baths
Catalysis production of high
purity nickel powder
Coloration of ceramics and glass,
intermediate in production of
other Ni chemicals
Electroplating baths
Ni - Cd battery manufacture
Catalysis
Production of paint pigments
Source: Antonsen and Springer, 1968.
C-19
-------
Table C-17. Nickel in POTW Sludge: Selected Urban Cities
o
1
ro
o
PLANT LOCATION
Indianapolis, IN
Cincinnati , Oil
Lewis ton, ML"
Atlanta, GA
St. Louis, MO
Pottstown, PA
Grand Rapids, MI
Ni concentration (pg/1)
AVERAGE FLOW (10 I/day) INFLUENT EFFLUENT SLUDGE
400
30
38
340
95
23
190
90
30
62
20
12
701
345
40
20
42
10
40
294
325
3343
3090
478
2567
1070
17000
27300
Source: EPA, 1980b; 1980c.
-------
Table C-18. Corrosion Rates of Nickel Alloys
Alloy (Ni%) Conditions Corrosion Rate (mpy)a
Hastelloy alloy B-2 (65) 99% acetic acid by wt 0.3
89% fonnic acid by wt 0.5
70% sulfuric acid by wt 9.0
Inconel 600 (76) 50% phosphoric acidc . 1.53
35% hydrofluoric acid, 38.0
60% sodium hydroxide 4.0
Nickel 200 (99.5) 50% caustic sodaf 1.1
70% caustic potash9 0.1
Incoloy 825 (41.8) 10% oxalic acid1? 20.0
10% maleic acid 0.1
Source: After Hughson, 1976
jVlil per year, 1 mi 1=0.001 inch.
Boiling acids, laboratory tests of 120 hour duration.
.30 day test. n
Acid temperature of 167 F.
^Boiling NaOH.
Atmospheric pressure, 266° F, 720 hour test duration.
^Liquid velocity 21.6 ft/min., 300° P.
^120 hour test.
120 hour test.
-------
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C S 3* 3 C S 3 S 3° 3* 3 C £ S 3333* 3 3— 3 9 ~ -• -• — 3 9 3 C 3
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IS 3 3OJ19333 tf>^^3^
r: ? _ tc ;
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C-24
-------
o
I
ro
en
Inadvertent
Sources
Hossil Fuel
Coinlimlion
16.230
Manufacture
5.780
• AslK'SlOS
Industry
TobiiCLO
Cuinluislion
1
Production
Consumptive
Stock* UseS
12/31/79
16.400
J
1
Miinnii Derations
10.600
Arnax Oiwralions
29.500
1
Imports
161.100
Slocks
1/1/79
15.000
Secondary
Production
12.000
1
^ Alloys
15/.000
^ Electroplating
^ 27.500
Industrial Processes
40.100 f
Chemicals and
1060
^-
*—
^ Ballorius
1500
fc—
*-
Exports
31.800
TOTAL
Environmental Releases (kky)
AIR WATER0 LAND TOTAL
IT) (S) POTW
8.990 150 150 7,030 16.170
neg 1 1 2.600 2.600
530 neg neij b30
neg 200 50 150 3.040 3.240
30 132 132 132 295
52 1.164 1.066 98 1.9G2 3.178
neg 322 4 10
409 neg1 b.3/0 5,780
1 neg neg niiij neg
6 14 1 13 3 20
9 688 411 275 5/0 1. 2/0
neg neg 1 1
10.030 2.350 1.810 540 20.710 33.090
Nolo: Fuolnolvs nexl
FIGURE C-1 ESTIMATED ENVIRONMENTAL RELEASES OF NICKEL IN 1979
FROM ITS INADVERTENT SOURCES. PRODUCTION. AND USE (kkg)a
-------
ro
en
figure C-1. (Concluded)
a) Total amount of nickel imported and produced minus that which Is stockpiled and exported is equal to the sum of lhat used
plus roloosed; numbers do not add duo to: rounding; unreportud (confidential data) amount of nickel produced as by-product
(NISO.) by select eleclrolytic copper refineries; and small quantities ol nickel-containing materials may have been
stockpiled from previous yours by industries and are therefore not Included In 1979 production figures; numbers from
environmental releases correspond to those in Table 3-1. Table 3-1 should be referred 1o for further details.
b) Numbers reported as amount of nickol released from listed operations.
c) T=total, (S)+(POTW)=T, whore S=surfaco waters and POTW=publIcly owned 1real moot works.
d) Coal and/or petroleum products combusted by electrical ulilities, industry, coke ovens, rosidonlial/commerclal users and
vehicles used for transportation.
o) Mosf coal-and oil-fired boilers released bottom ash and/or control device-collected flyasti wastes 1o tailings ponds which
were periodically dredged to land, Klein, jjt^jij_., 1975.
f) Includes prlamry and secondary ferrous and nonferrous smelting and refining; seo Table 3-7.
g) Includes wot and dry processes, seo Table 3-8.
h) Seo footnote Y, Table 3-1.
i) Significant levels of nickel have not been detected In wastewaters from cement manufacture, i.e., mean values for nickel
waste loadings were reported as zero, EPA, I973c.
-------
MATTE
AIR
AIR
SCRAP
CRUSHING, BLENDING
SOLIDS
PRESSURE
LEACHING
Underflow to
tailings pond
which is re-
cycled
COPPER
ELECTRO-
WINNING
COPPER METAL
MATTE GRANULATING,
GRINDING
ATMOSPHERIC LEACHING
AIR
t
LIQUID
COBALT REMOVAL
LIQUID
NICKEL REDUCTION
COBALT
PURIFICATION
LIQUID
AIR
NICKEL
BRIQUETTING
& SINTERING
NICKEL REMOVAL
ION EXCHANGE
To 1st
Stage
Cond.
Strip
COBALT
REDUCTION
NICKEL
METAL
SCAVENGING
(ION EXCHANGE)
SOLIDS
LIQUID
COBALT
BRIQUETTING
& SINTERING
AMMONIUM
SULPHATE
CRYSTALLIZATION
Strip
—•_ To Ist-stage
Cond.
» WATER
COBALT METAL
i
AMMONIUM SULPHATE
PRODUCT
Figure C-2. Nickel Recovery from Matte and Waste Disposal Sites (Hoppe, 1977)
C-27
-------
BLISTER
COPPER
ANODE
FURNACE
QUENCH
TANK
COPPER PRODUCT
ELECTROLYTIC
CELLS
STEAM
J
neg. SLIME
—"TO RECOVERY
HEATED ELECTROLYTE
HEAT
EXCHANGER
CONDENSATE
LIBERATOR
CELLS
EVAPORATOR
CENTRIFUGE
DRYER
N1SO,
Figure C-3, Generalized Flow Diagram of Electrolytic Copper Refinery (EPA, 1975a)
Negligible to mean <1 *
-------
PRIMARY
PRODUCERS
PRIMARY
IMPORTS
ALLOY
PRODUCERS
RUNAROUND
SCRAP
END
PRODUCTS
~L
FOUNDRIES
AND OTHER
MANUFACTURING
RUNAROUND
SCRAP
_ j
CONSUMERS
OF SHAPES AND CASTINGS
PROMPT INDUSTRIAL
SCRAP
NONFERROUS
SMELTERS
AND REFINERS
STEEL MILLS
RUNAROUND
SCRAP
SCRAP
IMPORTS
J
u J
__ J
OLD
SCRAP
SCRAP
COLLECTOR
SCRAP
BROKER
_ J
EXPORTS
Figure C-4. Market Flow Diaarar" of Old Nickel-Base Scrao (Matthews, 1979).
C-29
-------
(\
NEW-—^
ENGLAND'
o
I
to
o
%» tV> W-r o ,->.-».
WEST NORTH
'^W
-------
ALKALIN:
CLEAN
ALKALINE
RINSE
ACID DIP
PICKLING
RINSE
NICKEL
PLATE
TWO-STAGE
COUNTERFLOW
RINSE
_L
CHROME
PLATE
TWO-STAGE
COUNTERFLOW
RINSE
T
HOT WATER
RINSE
NEUTRALIZATION
AND
PRECIPITATION
CLARIFICATION
WASTEWATER
DISCHARGE
CHROME
REDUCTION
Figure C-6. Nickel-Chrome Plate Sequence (Lowenheim, 1979).
C-31
-------
MUNICIPAL SOLID WASTE
50±10
PARTICULATE EMISSIONS
GASEOUS EMISSIONS
1±0.3 "
ROCKING GRATE INCINERATOR
BOTTOM ASH
FLYASH
13=15 36±56
LANDFILL
QUENCH WATER
UNDISSOLVED
SOLIDS
QUENCH WATER
DISSOLVED
SOLIDS
SPRAY CHAMBER
WATER
UNDISSOLVED SOLIDS
SPRAY CHAMBER
WATER
DISSOLVED SOLIDS
0.002
0.008
0.1
MUNICIPAL SEWER SYSTEM
0.05
Figure C-7. Flow Diagram of a Municloal Incinerator (Law and Gordon, 1979)'
akg nickel per 920 kkg refuse/week.
C-32
-------
APPENDIX D. CALCULATION OF RESPIRA3LE NICKEL
CONCENTRATION FROM A 1000-Mtf
COAL-FIRED POWER PLANT
Table D-l shows Che assumptions used for the sample calculation.
The total amount of nickel emissions per year is assumed to be
1500 kg. This source strength is divided into three particle sizes
as follows.
Partic le Size (urn) 3ource Strength (%) Source Strength (kg/s)
1. 0.5 25 1.20 x 10~5
2. 3 60 2.85 x 10~5
3. 10 15 7.00 x 10~6
The settling velocity of particles is calculated using Stokes
formula i
Vs - ^ar (1)
13ua
where d = diameter, m
•5
"ar = average density of particles, kg/ra
'"a = dynamic viscosity of air, kg/ms
g - acceleration due to gravity, m/s
The calculated velocities are as follows
\'1 - 6.7 x 10~2 m/s
V2 - 2.4 x 10~3 m/s
V3 - 2.7 x 10~2 m/s
The source depletion is calculated using the procedure described
in Slade (1968). The source depletions in neutral atmosphere are shown
for initial source heights of 100 m and 10 ra, shown in Figure D-l. As
can be seen from the figure, the depletion is negligible for particulates
of diameter less than 3 m. Since nearly 85% of the source has a mean
diameter less than 3 m, the respirable concentration of nickel resulting
from coal-firsd power plants can be very high.
The centerline ground level concentration is given by
( 1 /H
exp < - - [ -~
D-l
-------
TABLE D-l. ASSUMPTION'S "OR SAMPLE CALCULATIONS OF NICKEL
EMISSIONS IN THE ATMOSPHERE
Power Plant Capacity
Coal Used
Type of Boiler
Total Coal Consumption
Total Fly Ash Generated
Total Nickel Emissions
Particulate Size
Stack Height
Atmospheric Stability
1000 MW
Subbituminous
Tangentially fired with electrostatic
precipitator3
.2.6 x 106 kkg/yr
1.3 x 103 kkg/yr
1500 kg/yr
25% of 0.5 \im diameter
60% of 3 um diameter
15% of 10 ym diameter
100 in
Neutral
This summary would not change significantly for different boilers
with the exception of stoker boiler for which the emissions would
be only slightly higher.
Source: Arthur D. Little, Inc.
D-2
-------
„
in
5
/ a a ^
; a o _
/ ° "~
/ I
/
/
/
/
fill
00 ffl 1
II ~
1
1
1
1
CN
— o' o o o
a
111
z
2
O
LU
U
GC
3
a
LU
E
=9
0
u
c
8
hi
3
°D/XD '°!
0-3
-------
• r . \
where 0 is the depeleted source strength corresponding to a particle
diameter d^ at distance x from the source. This can be obtained directly
fron Figure D-l. -^ and cz are Pasquill-C-if f ord dispersion coefficients.
The total anbient centerline concentration is given by
Ctotal(x) = Cl + C2 + C3
The total respirable concentration is given by
Cres(x) " Cl + C2
The total deposition rate is given by
w(x) - C.^ + C,V2 4- C3V3
Since Vj^ and V? are very small, the predominant contribution to
deposition comes from larger particles of greater settling velocities,
D-4
-------
REFERENCE
Slade, D.H.; ed. Meteorology and atomic energy. Washington, DC: U.S.
Atomic Energy Commission: 1968.
D-5
-------
-------
APPENDIX E. STORE! RIVER BASIN CODES
This appendix contains listings of the major river basin codes
which EPA has defined for the waterways within the United States.
There are 23 major river basins defined within the United States. The
listings are in order by major basin code.
A complete listing of these basin codes can also be obtained by
listing the STORET help data set named BASIN.CODES.
Major River Basins
CODE
01
02
03
04
05
06
07
08
09
10
11
12
13
14
15
16
17
18
19
20
21
22
23
NAME
NORTHEAST
NORTH ATLANTIC
SOUTHEAST
TENNESSEE RIVER
OHIO RIVER
LAKE ERIE
UPPER MISSISSIPPI RIVER
LAKE MICHIGAN
MISSOURI RIVER
SOUTH CENTRAL LOWER MISSISSIPPI RIVER
COLORADO RIVER
WESTERN GULF
PACIFIC NORTHWEST
CALIFORNIA
GREAT BASIN
ALASKA
HAWAII
PUERTO RICO
VIRGIN ISLANDS
OCEANIA
LAKE HURON
LAKE SUPERIOR
HUDSON BAY
E-l
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