Origins of Qualitative Risk
Management
Prior to the creation of OELs, most large
chemical manufacturers used qualitative
exposure assessment processes and qualitative health hazard reviews. Since the
early 1950s, for example, The Dow
Chemical Company has assigned risk
management control strategies based on
a “health effects rating.” Using these ratings in conjunction with information
about the degree, duration and frequency
of exposure, hygienists at Dow would
create a monitoring plan to verify that a
control strategy adequately controls exposures at the targeted levels.
The pharmaceutical industry has em-
braced control banding, also known as
performance-based exposure control limits
(PB-ECLs), extensively for over 20 years.
In the late 1980s, the pharmaceutical in-
dustry began using PB-ECLs and controls
to protect workers from exposure to drugs
with known therapeutic effects. The high
potency of some pharmaceutical com-
pounds required alternatives to setting
OELs, especially for early development
compounds with limited information. Be-
cause there are rarely R-phrases for these
drugs, utilization of the actual toxicity and
therapeutic data are used in a matrix.
Applications of Hazard Banding
Decoupling hazard banding from control
banding allows assessment of hazards to
be utilized in hazard communication and
awareness efforts after a substance has
been introduced in a workplace. Better
yet, the hazard assessment can aid the
substitution or design of controls. Although hazard banding is not a substitute
for OELs, it yields insight into the relative
toxicity of substances. Occupational hygienists can use this information to provide expert guidance for hazard ranking
and prioritization.
In the European Union—particularly in
applications of the toolkit provided by the
Figure 1. A hazard-band evaluation of Dichloracetic Acid using the matrix provided by eCOSHH.
Criterion
Virtually Non-Toxic
ND A
Low Toxicity
B
Moderate Toxicity
C
Toxic
D
High Toxicity
E
Comments/Rationale
Acute toxicity (Rat oral LD50)
300-2,000 mg/kg
50-300 mg/kg
5-50 mg/kg
< 5 mg/kg
Acute toxicity (Rat inhalation
LC50)- Not Available
Sensory irritation (RD50)-
Not Available
> 10,000 ppm
1000-10,000 ppm
100-1000 ppm
1-100 ppm
> 3,000 ppm
> 3,000 ppm
300-3000 ppm
30-300 ppm
1-30 ppm
Skin or eye irritation
mild to moderate
moderate to severe severe to corrosive
corrosive
corrosive
Extrapolated from
comments only
Corrosive to respiratory tract
Corrosive to eyes, skin and
respiratory tract; Inhalation of high concentra-
tions can cause pulmonary edema
Irritation threshold (ppm)-
Not Available
x
>1000
<1
Target organ toxicity NOEL
Neurotoxicity
>1000 ppm
>100 mg/kg/d
>1000 ppm
10-100 mg/kg/d
10-100 ppm
0.1-1 mg/kg/d
1-10 ppm
<0.1 mg/kg/d
Severity of target organ toxicity
100-1000 10-100 1-10
100-1000 ppm
1-10 mg/kg/d
Moser: 16 mg/kg/d
LOAEL Neurotox
severity of the toxicity can push the above NOEL into a higher cell
Repro/dev tox NOEL
>300 mg/kg/d
30-300 mg/kg/d
3-30 mg/kg/d
0. 3-3 mg/kg/d
LOAEL 12. 5 mg/kg/d
(90d study in dogs)
<0.3 mg/kg/d
LOAEL 12. 5 mg/kg/day (sodium salt) in
dogs 90 day study showed degeneration
of testicular germinal cell epithelium and
syncytial giant cell formation
Reproductive toxicity
severity of the toxicity can push the above NOEL into a higher cell
Developmental toxicity
14 mg/kg/day was identified as a NOAEL
for dev. Tox
Genetox
negative
Cancer dose-NOEL/NOAELs
Carcinogenicity potential
Warning properties / odor
OEL range (mcg/m3 and ppm)
severity of the toxicity can push the above NOEL into a higher cell
equivocal likely / limited or based on in vitro positive WOE including in vivo
30-300 mg/kg/d 3-30 mg/kg/d 0. 3-3 mg/kg/d
severity of the toxicity can push the above NOEL into a higher cell
good fair to none poor to none
≥100, <1000 ≥ 10, <100 ≥1, < 10
Yes
LD50=510 mg/kg
Yes
positive WOE
and potent
<0.3 mg/kg/d
good: 0.04 ppm
greater than 200 mg/kd
Sensitization notation
No
