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EC number: 205-563-8
CAS number: 142-82-5
Short description of key information on bioaccumulation potential result: See toxicokinetics, metabolism and distribution.Short description of key information on absorption rate: Under dermal in vitro test conditions, heptane was able to penetrate the skin. During prolonged exposure, the penetration of the skin was aggravated, since the exposure to heptane simultaneously reduced skin barrier function.Due to the experimental setup, e. g. undepletable reservoir of test substance and therefore absence of any evaporation, the dermal penetration factors reported by Fasano and McDougal (2008) are very conservative. In contrast, when using a diffusion cell, which is a more realistic setup for volatile subsances like hydrocarbon solvents, dermal penetration rates of 0.1 µg/cm2/h and 0.0005 µg/cm2/h were obtained for heptane and octane, respectively (Tsuruta et al., 1982).
The uptake of inhaled Normal-Heptane
vapors was explored by Dahl et al. (1988) in male rats exposed for 5
consecutive days, 80 min/day with escalation of vapor concentration
daily (from 1 ppm up to 5000 ppm). During the exposures, respiratory and
gas chromatographic data were collected at 1 min intervals. For
Normal-Heptane, only data from one exposure at 100 ppm were available.
Uptake of inhaled heptane vapor was 4.5 ± 0.3 nmol/kg/min/ppm (n = 10).
The value is given for uptake during minutes 60 to 70 from the start of
exposure of the experiment.
of Normal-Heptane were investigated in rats during inhalation of 100 ppm
of the hydrocarbon for 3 days, 12 hours/day (Zahlsen et al., 1992). The
concentration of Normal-Heptane was measured by head space gas
chromatography in blood, brain, liver, kidneys and perirenal fat.
Normal-Heptane was found in moderate concentrations in the kidneys and
only in marginal concentrations in blood, brain and liver. In perirenal
fat, concentrations were the highest, however, decreasing with lasting
exposure. This is in contrast to other n-alkanes, which showed
of Normal-Heptane were determined in human blood and tissues by
Perbellini et al. (1985). The solubility of heptane was tested in blood,
saline, olive oil and in the most important human tissues (lung, kidney,
liver, brain, muscle, heart, and fat). The solubility of Normal-Heptane
in saline was low and very high in olive oil, displaying a partition
coefficient of 452 (20.0 SD). The partition coefficients were therefore
high in fat and fatty tissues compared to the other examined tissues.
Alkanes that are
metabolized to gamma diketones can produce peripheral neuropathy in
experimental animals and man. Perbellini et al. (1986) have demonstrated
that C7-C9 n-alkanes do not generate neurotoxic metabolites or produce
them in quantities too low to produce neurotoxic effects. Exposure of
male rats to 1800 ppm Normal-Heptane for 6 hours only produced the major
urinary metabolites 2-heptanol and 3-heptanol. 2,5-Heptanedione, a
potentially neurotoxic metabolite was only present in a low
concentration (4.4 µg/24 hours) in the urine, approximately 0.8% of
urinary metabolites. Other metabolites included 2- or 3-heptanone and
gamma valerolactone. At the end of exposure, the amount of 2-heptanol in
blood and tissue (liver, muscle, kidney, and nervous tissue) was between
0.2 and 2.0 mg/L. The concentration of the parent compound Normal-Heptane
was 5.7 mg/L in blood and 10 to 25.6 mg/L in tissues. 24 hours after the
end of exposure, no quantifiable amounts were present in blood or
tissue, demonstrating rapid clearance of Normal-Heptane and its
Discussion on bioaccumulation potential result:
See toxicokinetics, metabolism and distribution.
Discussion on absorption rate:
Fasano and McDougal (2008) described
the procedures for determination of a permeability coefficient (Kp) and
two short-term dermal absorption rates at 10 and 60 min. The flux values
for heptane and the 10 and 60 min short-term absorption values (the
quantity of chemical remaining in the skin plus that portion that had
penetrated the skin was detected in the receptor fluid) were 63.2
µg/cm2/h, 113 µg/cm2/h (for the 10 min flux) and 22.1 µg/cm2/h (for the
60 min flux). Therefore, the 10 min flux value for heptane (based on
both the amount in the skin and the receptor solution) was greater than
the flux measured in a similar manner over 60 min.
Skin integrity measurements were taken
before and after each experiment. A ratio of post- to pre-test impedance
of "1" indicates that the skin barrier did not change over the course of
the experiment. In the Kp experiments, skin exposed to Normal-Heptane
had a damage ratio of 0.57, confirming that approx. 43% of the skin
barrier function was lost due to exposure to heptane. The barrier
properties for the skin in the short-term experiments were given as the
ratios of 0.90 for 10 min and 0.88 for 60 min. At the end of the Kp
experiment, the portion of Normal-Heptane in the skin (0.01%) was less
than the portion in the receptor solution (0.12%). The portion of Normal-Heptane
in the donor solution (wash) was 95.4%. In contrast to the Kp
experiment, the skin (0.14%) retained a larger percentage of Normal-Heptane
following a 10 min exposure. The portion of Normal-Heptane in the donor
solution (wash) was 6.84% at 10 min. The greater portion of the applied
dose remaining in the skin at 10 min suggests that partitioning into the
skin from the donor solution is the driver of penetration with this
brief exposure. After the 60 min experiments, there was also a larger
percentage of heptane in the receptor solution (0.12%) than in the skin
(0.06%). The increased proportion of Normal-Heptane detected in the
receptor solution illustrates and confirms the movement of the chemical
from the skin into the receptor solution. Under the test conditions, Normal-Heptane
was able to penetrate the skin. During prolonged exposure, the
penetration of the skin was aggravated, since the exposure to heptane
simultaneously reduced skin barrier function.
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